EcoliWiki - User contributions [en]

PMID:19377097

2011-08-19T19:42:22Z

Mdmueller: /* See also */

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<protect>
 '''Graham, AI, Hunt, S, Stokes, SL, Bramall, N, Bunch, J, Cox, AG, McLeod, CW and Poole, RK''' (2009) Severe zinc depletion of Escherichia coli: roles for high affinity zinc binding by ZinT, zinc transport and zinc-independent proteins.''J. Biol. Chem.'' '''284''':18377-89

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|{{TableHeadingColor}} |'''Abstract''' || <protect>Zinc ions play indispensable roles in biological chemistry. However, bacteria have an impressive ability to acquire Zn(2+) from the environment, making it exceptionally difficult to achieve Zn(2+) deficiency, and so a comprehensive understanding of the importance of Zn(2+) has not been attained. Reduction of the Zn(2+) content of Escherichia coli growth medium to 60 nm or less is reported here for the first time, without recourse to chelators of poor specificity. Cells grown in Zn(2+)-deficient medium had a reduced growth rate and contained up to five times less cellular Zn(2+). To understand global responses to Zn(2+) deficiency, microarray analysis was conducted of cells grown under Zn(2+)-replete and Zn(2+)-depleted conditions in chemostat cultures. Nine genes were up-regulated more than 2-fold (p < 0.05) in cells from Zn(2+)-deficient chemostats, including zinT (yodA). zinT is shown to be regulated by Zur (zinc uptake regulator). A mutant lacking zinT displayed a growth defect and a 3-fold lowered cellular Zn(2+) level under Zn(2+) limitation. The purified ZinT protein possessed a single, high affinity metal-binding site that can accommodate Zn(2+) or Cd(2+). A further up-regulated gene, ykgM, is believed to encode a non-Zn(2+) finger-containing paralogue of the Zn(2+) finger ribosomal protein L31. The gene encoding the periplasmic Zn(2+)-binding protein znuA showed increased expression. During both batch and chemostat growth, cells "found" more Zn(2+) than was originally added to the culture, presumably because of leaching from the culture vessel. Zn(2+) elimination is shown to be a more precise method of depleting Zn(2+) than by using the chelator N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine.</protect>
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|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=19377097 PubMed]
Online version:[http://dx.doi.org/10.1074/jbc.M109.001503 10.1074/jbc.M109.001503]
|}
</protect>
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<protect>

{| id="F4c802d5212069" class=" tableEdit GO_table_reference"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.176069.F4c802d5212069&page=176069&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
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</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
#[http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE11894 GEO Accession: GSE11894]
#[http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-11894 ArrayExpress Accession: E-GEOD-11894]

==References==
{{RefHelp}}
<references/>

PMID:17921306

2011-08-18T19:54:06Z

Mdmueller: /* See also */

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<protect>
 '''Hobman, JL, Patel, MD, Hidalgo-Arroyo, GA, Cariss, SJ, Avison, MB, Penn, CW and Constantinidou, C''' (2007) Comparative genomic hybridization detects secondary chromosomal deletions in Escherichia coli K-12 MG1655 mutants and highlights instability in the flhDC region.''J. Bacteriol.'' '''189''':8786-92

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|{{TableHeadingColor}} |'''Abstract''' || <protect>The use of whole-genome microarrays for monitoring mutagenized or otherwise engineered genetic derivatives is a potentially powerful tool for checking genomic integrity. Using comparative genomic hybridization of a number of unrelated, directed deletion mutants in Escherichia coli K-12 MG1655, we identified unintended secondary genomic deletions in the flhDC region in delta fnr, delta crp, and delta creB mutants. These deletions were confirmed by PCR and phenotypic tests. Our findings show that nonmotile progeny are found in some MG1655 directed deletion mutants, and studies on the effects of gene knockouts should be viewed with caution when the mutants have not been screened for the presence of secondary deletions or confirmed by other methods.</protect>
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|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=17921306 PubMed]
Online version:[http://dx.doi.org/10.1128/JB.00977-07 10.1128/JB.00977-07]
|}
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<protect>

{| id="D4e4d6d7a85f99" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.179819.D4e4d6d7a85f99&page=179819&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
#[http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE7695 GEO Accession: GSE7695]
#[http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-7695 ArrayExpress Accession E-GEOD-7695]

==References==
{{RefHelp}}
<references/>

PMID:17921306

2011-08-18T19:53:30Z

Mdmueller: /* See also */

PMID:17921306

2011-08-18T19:52:26Z

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PMID:17921306

2011-08-18T19:52:26Z

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PMID:19635828

2011-08-11T21:26:27Z

Mdmueller: /* See also */

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<protect>
 '''Tree, JJ, Wang, D, McInally, C, Mahajan, A, Layton, A, Houghton, I, Elofsson, M, Stevens, MP, Gally, DL and Roe, AJ''' (2009) Characterization of the effects of salicylidene acylhydrazide compounds on type III secretion in Escherichia coli O157:H7.''Infect. Immun.'' '''77''':4209-20

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|{{TableHeadingColor}} |'''Abstract''' || <protect>Recent work has highlighted a number of compounds that target bacterial virulence by affecting gene regulation. In this work, we show that small-molecule inhibitors affect the expression of the type III secretion system (T3SS) of Escherichia coli O157:H7 in liquid culture and when this bacterium is attached to bovine epithelial cells. Inhibition of T3SS expression resulted in a reduction in the capacity of the bacteria to form attaching and effacing lesions. Our results show that there is marked variation in the abilities of four structurally related compounds to inhibit the T3SS of a panel of isolates. Using transcriptomics, we performed a comprehensive analysis of the conserved and inhibitor-specific transcriptional responses to these four compounds. These analyses of gene expression show that numerous virulence genes, located on horizontally acquired DNA elements, are affected by the compounds, but the number of genes significantly affected varied markedly for the different compounds. Overall, we highlight the importance of assessing the effect of such "antivirulence" agents on a range of isolates and discuss the possible mechanisms which may lead to the coordinate downregulation of horizontally acquired virulence genes.</protect>
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|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=19635828 PubMed]
Online version:[http://dx.doi.org/10.1128/IAI.00562-09 10.1128/IAI.00562-09]
|}
</protect>
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{{LitMaterials}}

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<protect>

{| id="N4e4448b229908" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.179707.N4e4448b229908&page=179707&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
#[http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE10319 GEO Accession: GSE10319]
#[http://www.ebi.ac.uk/arrayexpress/Experiments/E-GEOD-10319 ArrayExpress Accession: E-GEOD-10319]

==References==
{{RefHelp}}
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PMID:19635828

2011-08-11T21:25:06Z

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PMID:19635828

2011-08-11T21:25:05Z

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PMID:19759044

2011-08-11T17:50:40Z

Mdmueller: /* See also */

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<protect>
 '''Bailey, AM, Constantinidou, C, Ivens, A, Garvey, MI, Webber, MA, Coldham, N, Hobman, JL, Wain, J, Woodward, MJ and Piddock, LJ''' (2009) Exposure of Escherichia coli and Salmonella enterica serovar Typhimurium to triclosan induces a species-specific response, including drug detoxification.''J. Antimicrob. Chemother.'' '''64''':973-85

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|{{TableHeadingColor}} |'''Abstract''' || <protect>The use of triclosan within various environments has been linked to the development of multiple drug resistance (MDR) through the increased expression of efflux pumps such as AcrAB-TolC. In this work, we investigate the effect of triclosan exposure in order to ascertain the response of two species to the presence of this widely used biocide.</protect>
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|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=19759044 PubMed]
Online version:[http://dx.doi.org/10.1093/jac/dkp320 10.1093/jac/dkp320]
|}
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<protect>

{| id="M4e4415fe7c887" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.179696.M4e4415fe7c887&page=179696&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
#[http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE15059 GEO Accession: GSE15059]
#[http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-15059 ArrayExpress Accession: E-GEOD-15059]

==References==
{{RefHelp}}
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PMID:19759044

2011-08-11T17:48:46Z

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PMID:19759044

2011-08-11T17:48:46Z

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PMID:17635554

2011-08-11T17:47:42Z

Mdmueller: /* See also */

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<protect>
 '''Tree, JJ, Ulett, GC, Hobman, JL, Constantinidou, C, Brown, NL, Kershaw, C, Schembri, MA, Jennings, MP and McEwan, AG''' (2007) The multicopper oxidase (CueO) and cell aggregation in Escherichia coli.''Environ. Microbiol.'' '''9''':2110-6

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|{{TableHeadingColor}} |'''Abstract''' || <protect>cueO encodes a periplasmic multicopper oxidase, which is known to be involved in copper homeostasis and protection against oxidative stress in Escherichia coli K12. Transcriptional profiling showed that expression of genes associated with motility was lowered in a cueO mutant while expression of genes associated with autoaggregation was elevated. Increased aggregation was correlated with increased expression of cell surface proteins antigen 43 and curli. Changes in gene expression caused by the deletion of cueO were essentially independent of SoxR and OxyR, the global regulators of oxidative stress response.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=17635554 PubMed]
Online version:[http://dx.doi.org/10.1111/j.1462-2920.2007.01320.x 10.1111/j.1462-2920.2007.01320.x]
|}
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{{LitMaterials}}

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<protect>

{| id="Y4e4414f3cac62" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.179695.Y4e4414f3cac62&page=179695&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
#[http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE5177 GEO Accession: GSE5177]
#[http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-5177 ArrayExpress Accession: E-GEOD-5177]

==References==
{{RefHelp}}
<references/>

PMID:17635554

2011-08-11T17:47:15Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''Tree, JJ, Ulett, GC, Hobman, JL, Constantinidou, C, Brown, NL, Kershaw, C, Schembri, MA, Jennings, MP and McEwan, AG''' (2007) The multicopper oxidase (CueO) and cell aggregation in Escherichia coli.''Environ. Microbiol.'' '''9''':2110-6

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>cueO encodes a periplasmic multicopper oxidase, which is known to be involved in copper homeostasis and protection against oxidative stress in Escherichia coli K12. Transcriptional profiling showed that expression of genes associated with motility was lowered in a cueO mutant while expression of genes associated with autoaggregation was elevated. Increased aggregation was correlated with increased expression of cell surface proteins antigen 43 and curli. Changes in gene expression caused by the deletion of cueO were essentially independent of SoxR and OxyR, the global regulators of oxidative stress response.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=17635554 PubMed]
Online version:[http://dx.doi.org/10.1111/j.1462-2920.2007.01320.x 10.1111/j.1462-2920.2007.01320.x]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

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{{LitMaterials}}

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<protect>

{| id="Y4e4414f3cac62" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.179695.Y4e4414f3cac62&page=179695&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
#[http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GE5177 GEO Accession: GSE5177]
#[http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-5177 ArrayExpress Accession: E-GEOD-5177]

==References==
{{RefHelp}}
<references/>

PMID:15466047

2011-08-04T17:56:08Z

Mdmueller: /* See also */

{{RightTOC}}

 '''Grainger, DC, Overton, TW, Reppas, N, Wade, JT, Tamai, E, Hobman, JL, Constantinidou, C, Struhl, K, Church, G and Busby, SJ''' (2004) Genomic studies with Escherichia coli MelR protein: applications of chromatin immunoprecipitation and microarrays.''J. Bacteriol.'' '''186''':6938-43

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|{{TableHeadingColor}} |'''Abstract''' || Escherichia coli MelR protein is a transcription activator that is essential for melibiose-dependent expression of the melAB genes. We have used chromatin immunoprecipitation to study the binding of MelR and RNA polymerase to the melAB promoter in vivo. Our results show that MelR is associated with promoter DNA, both in the absence and presence of the inducer melibiose. In contrast, RNA polymerase is recruited to the melAB promoter only in the presence of inducer. The MelR DK261 positive control mutant binds to the melAB promoter but cannot recruit RNA polymerase. Further analysis of immunoprecipitated DNA, by using an Affymetrix GeneChip array, showed that the melAB promoter is the major, if not the sole, target in E. coli for MelR. This was confirmed by a transcriptomics experiment to analyze RNA in cells either with or without melR.
</noinclude>
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|{{TableHeadingColor}} nowrap |'''Links''' || [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15466047 PubMed]
|}

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{{LitSignificance}}

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{{LitMaterials}}

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{| id="S47a93bc37c1c1" class=" tableEdit GO_table_reference"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.0.S47a93bc37c1c1&page=0&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}


==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
*[http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE1421 at GEO]
*[http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-1421 ArrayExpress Accession E-GEOD-1421]

==References==
{{RefHelp}}
<references/>

PMID:15466047

2011-08-04T17:55:49Z

Mdmueller: /* See also */

{{RightTOC}}

 '''Grainger, DC, Overton, TW, Reppas, N, Wade, JT, Tamai, E, Hobman, JL, Constantinidou, C, Struhl, K, Church, G and Busby, SJ''' (2004) Genomic studies with Escherichia coli MelR protein: applications of chromatin immunoprecipitation and microarrays.''J. Bacteriol.'' '''186''':6938-43

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || Escherichia coli MelR protein is a transcription activator that is essential for melibiose-dependent expression of the melAB genes. We have used chromatin immunoprecipitation to study the binding of MelR and RNA polymerase to the melAB promoter in vivo. Our results show that MelR is associated with promoter DNA, both in the absence and presence of the inducer melibiose. In contrast, RNA polymerase is recruited to the melAB promoter only in the presence of inducer. The MelR DK261 positive control mutant binds to the melAB promoter but cannot recruit RNA polymerase. Further analysis of immunoprecipitated DNA, by using an Affymetrix GeneChip array, showed that the melAB promoter is the major, if not the sole, target in E. coli for MelR. This was confirmed by a transcriptomics experiment to analyze RNA in cells either with or without melR.
</noinclude>
|-
|{{TableHeadingColor}} nowrap |'''Links''' || [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15466047 PubMed]
|}

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{{LitSignificance}}

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{{LitMaterials}}

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{| id="S47a93bc37c1c1" class=" tableEdit GO_table_reference"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.0.S47a93bc37c1c1&page=0&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}


==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
*[http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE1421 at GEO]
*[[http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-1421 ArrayExpress Accession E-GEOD-1421]

==References==
{{RefHelp}}
<references/>

PMID:19346340

2011-08-02T16:37:42Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''Bergholz, TM, Vanaja, SK and Whittam, TS''' (2009) Gene expression induced in Escherichia coli O157:H7 upon exposure to model apple juice.''Appl. Environ. Microbiol.'' '''75''':3542-53

{|{{Prettytable}} align = 'center' width= '70%'
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|{{TableHeadingColor}} |'''Abstract''' || <protect>Escherichia coli O157:H7 has caused serious outbreaks of food-borne illness via transmission in a variety of food vehicles, including unpasteurized apple juice, dried salami, and spinach. To understand how this pathogen responds to the multiple stresses of the food environment, we compared global transcription patterns before and after exposure to model apple juice. Transcriptomes of mid-exponential- and stationary-phase cells were evaluated after 10 min in model apple juice (pH 3.5) using microarrays probing 4,886 open reading frames. A total of 331 genes were significantly induced upon exposure of cells to model apple juice, including genes involved in the acid, osmotic, and oxidative stress responses as well as the envelope stress response. Acid and osmotic stress response genes, including asr, osmC, osmB, and osmY, were significantly induced in response to model apple juice. Multiple envelope stress responses were activated as evidenced by increased expression of CpxR and Rcs phosphorelay-controlled genes. Genes controlled by CpxR (cpxP, degP, and htpX) were significantly induced 2- to 15-fold upon exposure to apple juice. Inactivation of CpxRA resulted in a significant decrease in survival of O157:H7 in model apple juice compared to the isogenic parent strain. Of the 331 genes induced in model apple juice, 104 are O157-specific genes, including those encoding type three secretion effectors (espJ, espB, espM2, espL3, and espZ). Elucidating the response of O157:H7 to acidic foods provides insight into how this pathogen is able to survive in food matrices and how exposure to foods influences subsequent transmission and virulence.</protect>
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|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=19346340 PubMed]
Online version:[http://dx.doi.org/10.1128/AEM.02841-08 10.1128/AEM.02841-08]
|}
</protect>
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<protect>

{| id="R4e382760d5637" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.179372.R4e382760d5637&page=179372&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
#[http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE11052 GEO Accession GSE11052]
#[http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-11052 ArrayExpress Accession E-GEOD-11052]

==References==
{{RefHelp}}
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PMID:19346340

2011-08-02T16:36:49Z

Mdmueller: /* See also */

PMID:19346340

2011-08-02T16:35:45Z

Mdmueller: Fill PMID: Page!

PMID:19346340

2011-08-02T16:35:44Z

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PMID:16141204

2011-07-26T19:23:42Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''Kao, KC, Tran, LM and Liao, JC''' (2005) A global regulatory role of gluconeogenic genes in Escherichia coli revealed by transcriptome network analysis.''J. Biol. Chem.'' '''280''':36079-87

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>In bacterial adaptation to the dynamic environment, metabolic genes are typically thought to be the executors, whereas global transcription regulators are regarded as the decision makers. Although the feedback from metabolic consequence is believed to be important, much less is understood. This work demonstrates that the gluconeogenic genes in Escherichia coli, ppsA, sfcA, and maeB, provide a feedback loop to the global regulator, cAMP receptor protein (CRP), in carbon source transition. Disruption of one of the gluconeogenic pathways has no phenotype in balanced growth, but causes a significant delay in the diauxic transition from glucose to acetate. To investigate the underlying mechanism, we measured the transcriptome profiles during the transition using DNA microarray, and network component analysis was employed to obtain the transcription factor activities. Results showed that one of the global regulators, CRP, was insufficiently activated during the transition in the ppsA deletion mutant. Indeed, addition of cAMP partially rescued the delay in transition. These results suggest that the gluconeogenic flux to phosphoenolpyruvate is important for full activation of adenylate cyclase through the phosphorylated enzyme IIA(glu) of the phosphotransferase system. Reduction of this flux causes insufficient activation of CRP and a global metabolic deficiency, which exemplifies a significant feedback interaction from metabolism to the a global regulatory system.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16141204 PubMed]
Online version:[http://dx.doi.org/10.1074/jbc.M508202200 10.1074/jbc.M508202200]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{| id="P4e2f13c3d3fb4" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.178928.P4e2f13c3d3fb4&page=178928&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
#[http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-3250 ArrayExpress Accession E-GEOD-3250]
#[http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE3250 GEO Page GSE3250]

==References==
{{RefHelp}}
<references/>

PMID:16799466

2011-07-19T17:08:31Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''Blot, N, Mavathur, R, Geertz, M, Travers, A and Muskhelishvili, G''' (2006) Homeostatic regulation of supercoiling sensitivity coordinates transcription of the bacterial genome.''EMBO Rep.'' '''7''':710-5

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>Regulation of cellular growth implies spatiotemporally coordinated programmes of gene transcription. A central question, therefore, is how global transcription is coordinated in the genome. The growth of the unicellular organism Escherichia coli is associated with changes in both the global superhelicity modulated by cellular topoisomerase activity and the relative proportions of the abundant DNA-architectural chromatin proteins. Using a DNA-microarray-based approach that combines mutations in the genes of two important chromatin proteins with induced changes of DNA superhelicity, we demonstrate that genomic transcription is tightly associated with the spatial distribution of supercoiling sensitivity, which in turn depends on chromatin proteins. We further demonstrate that essential metabolic pathways involved in the maintenance of growth respond distinctly to changes of superhelicity. We infer that a homeostatic mechanism organizing the supercoiling sensitivity is coordinating the growth-phase-dependent transcription of the genome.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16799466 PubMed]
Online version:[http://dx.doi.org/10.1038/sj.embor.7400729 10.1038/sj.embor.7400729]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{| id="U4e00c7c5d178e" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.177958.U4e00c7c5d178e&page=177958&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
# [http://www.ebi.ac.uk/arrayexpress/experiments/E-MEXP-462 ArrayExpress Accession E-MEXP-462]
# [http://www.ebi.ac.uk/arrayexpress/experiments/E-MEXP-464 ArrayExpress Accession E-MEXP-464]
# [http://www.ebi.ac.uk/arrayexpress/experiments/E-MEXP-465 ArrayExpress Accession E-MEXP-465]

==References==
{{RefHelp}}
<references/>

PMID:15659689

2011-07-19T17:04:28Z

Mdmueller: /* See Also */

{{RightTOC}}

 '''Lee, LJ, Barrett, JA and Poole, RK''' (2005) Genome-wide transcriptional response of chemostat-cultured Escherichia coli to zinc.''J. Bacteriol.'' '''187''':1124-34

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || Zinc is an essential trace metal ion for growth, but an excess of Zn is toxic and microorganisms express diverse resistance mechanisms. To understand global bacterial responses to excess Zn, we conducted transcriptome profiling experiments comparing Escherichia coli MG1655 grown under control conditions and cells grown with a toxic, sublethal ZnSO4 concentration (0.2 mM). Cultures were grown in a defined medium lacking inorganic phosphate, permitting maximum Zn bioavailability, and in glycerol-limited chemostats at a constant growth rate and pH. Sixty-four genes were significantly up-regulated by Zn stress, including genes known to be involved in Zn tolerance, particularly zntA, zraP, and hydG. Microarray transcriptome profiling was confirmed by real-time PCR determinations of cusF (involved in Ag and Cu efflux), ais (an Al-inducible gene), asr (encoding an acid shock-inducible periplasmic protein), cpxP (a periplasmic chaperone gene), and basR. Five up-regulated genes, basR and basS [encoding a sensor-regulator implicated in Salmonella in Fe(III) sensing and antibiotic resistance], fliM (flagellar synthesis), and ycdM and yibD (both with unknown functions), are important for growth resistance to zinc, since mutants with mutations in these genes exhibited zinc sensitivity in liquid media and on metal gradient plates. Fifty-eight genes were significantly down-regulated by Zn stress; notably, several of these genes were involved in protection against acid stress. Since the mdt operon (encoding a multidrug resistance pump) was also up-regulated, these findings have important implications for understanding not only Zn homeostasis but also how bacterial antibiotic resistance is modulated by metal ions.
</noinclude>
|-
|{{TableHeadingColor}} nowrap |'''Links''' || [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15659689 PubMed]
|}

==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==


{| id="F47ab8af78a860" class=" tableEdit GO_table_reference"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.0.F47ab8af78a860&page=0&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}


==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See Also==
# [http://www.ebi.ac.uk/arrayexpress/experiments/E-MEXP-222 ArrayExpress Accession E-MEXP-222]

==References==
{{RefHelp}}
<references/>

PMID:19833773

2011-07-19T16:59:22Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''Weber, MM, French, CL, Barnes, MB, Siegele, DA and McLean, RJ''' (2010) A previously uncharacterized gene, yjfO (bsmA), influences Escherichia coli biofilm formation and stress response.''Microbiology (Reading, Engl.)'' '''156''':139-47

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>Bacteria growing as surface-adherent biofilms are better able to withstand chemical and physical stresses than their unattached, planktonic counterparts. Using transcriptional profiling and quantitative PCR, we observed a previously uncharacterized gene, yjfO to be upregulated during Escherichia coli MG1655 biofilm growth in a chemostat on serine-limited defined medium. A yjfO mutant, developed through targeted-insertion mutagenesis, and a yjfO-complemented strain, were obtained for further characterization. While bacterial surface colonization levels (c.f.u. cm(-2)) were similar in all three strains, the mutant strain exhibited reduced microcolony formation when observed in flow cells, and greatly enhanced flagellar motility on soft (0.3 %) agar. Complementation of yjfO restored microcolony formation and flagellar motility to wild-type levels. Cell surface hydrophobicity and twitching motility were unaffected by the presence or absence of yjfO. In contrast to the parent strain, biofilms from the mutant strain were less able to resist acid and peroxide stresses. yjfO had no significant effect on E. coli biofilm susceptibility to alkali or heat stress. Planktonic cultures from all three strains showed similar responses to these stresses. Regardless of the presence of yjfO, planktonic E. coli withstood alkali stress better than biofilm populations. Complementation of yjfO restored viability following exposure to peroxide stress, but did not restore acid resistance. Based on its influence on biofilm maturation and stress response, and effects on motility, we propose renaming the uncharacterized gene, yjfO, as bsmA (biofilm stress and motility).</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=19833773 PubMed]
Online version:[http://dx.doi.org/10.1099/mic.0.031468-0 10.1099/mic.0.031468-0]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{| id="U4c48989960738" class=" tableEdit GO_table_reference"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.173130.U4c48989960738&page=173130&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
#[http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-18362 ArrayExpress Accession: E-GEOD-18362]
#[http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE18362 GEO Page: E-GEOD-18362]

==References==
{{RefHelp}}
<references/>

PMID:17600050

2011-07-19T16:56:45Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''Ihssen, J, Grasselli, E, Bassin, C, François, P, Piffaretti, JC, Köster, W, Schrenzel, J and Egli, T''' (2007) Comparative genomic hybridization and physiological characterization of environmental isolates indicate that significant (eco-)physiological properties are highly conserved in the species Escherichia coli.''Microbiology (Reading, Engl.)'' '''153''':2052-66

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>Escherichia coli, the common inhabitant of the mammalian intestine, exhibits considerable intraspecies genomic variation, which has been suggested to reflect adaptation to different ecological niches. Also, regulatory trade-offs, e.g. between catabolic versatility and stress protection, are thought to result in significant physiological differences between strains. For these reasons, the relevance of experimental observations made for 'domesticated' E. coli strains with regard to the behaviour of this species in its natural environments is often questioned and doubts are frequently raised on the status of E. coli as a defined species. The variability of important (eco-)physiological functions, such as carbon substrate uptake and breakdown capabilities, as well as stress defence mechanisms, in the genomes of commensal and pathogenic E. coli strains were therefore investigated. Furthermore, (eco-)physiological properties of environmental strains were compared to standard laboratory strain K-12 MG1655. Catabolic, stress protection, and carbon- and energy source transport operons showed a very low intraspecies variability in 57 commensal and pathogenic E. coli. Environmental isolates adapted to glucose-limited growth in a similar way as E. coli MG1655, namely by increasing their catabolic flexibility and by inducing high-affinity substrate uptake systems. The results obtained indicate that significant (eco-)physiological properties are highly conserved in the natural population of E. coli. This questions the proposed dominant role of horizontal gene transfer for niche adaptation.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=17600050 PubMed]
Online version:[http://dx.doi.org/10.1099/mic.0.2006/002006-0 10.1099/mic.0.2006/002006-0]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{| id="B4e00c27d75023" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.177957.B4e00c27d75023&page=177957&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE6407 GEO Page: E-GEOD-6407]
# [http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-6407 ArrayExpress Accession E-GEOD-6407]

==References==
{{RefHelp}}
<references/>

PMID:16913923

2011-07-19T16:53:51Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''Berney, M, Weilenmann, HU and Egli, T''' (2006) Gene expression of Escherichia coli in continuous culture during adaptation to artificial sunlight.''Environ. Microbiol.'' '''8''':1635-47

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>Escherichia coli growing in continuous culture under continuous UVA irradiation exhibits growth inhibition with a subsequent adaptation to the stress. Transcriptome analysis was performed during transient growth inhibition and in the UVA light-adapted growth state. The results indicate that UVA light induces stringent response and an additional response that includes the upregulation of the synthesis of valine, isoleucine, leucine, phenylalanine, histidine and glutamate. The induction of several SOS response-genes strongly points to DNA damage as a result of UVA exposure. The involvement of oxidative stress was observed with the induction of ahpCF. Taken together it supports the hypothesis of the production of reactive oxygen species by UVA light. In the UVA-adapted cell population strong repression of the acid tolerance response was found. We identified the enzyme chorismate mutase as a possible chromophore for UVA light-inactivation and found strong repression of the pyrBI operon and the gene mgtA encoding for an ATP-dependent Mg2+ transporter. Furthermore, our results indicate that the role of RpoS may not be as important in the adaptation of E. coli to UVA light as it was implicated by previous results with starved cells, but that RpoS might be of crucial importance for the resistance under transient light exposure.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16913923 PubMed]
Online version:[http://dx.doi.org/10.1111/j.1462-2920.2006.01057.x 10.1111/j.1462-2920.2006.01057.x]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{| id="J4e00c153e967b" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.177956.J4e00c153e967b&page=177956&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
#[http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE4569 GEO Page: E-GEOD-4569]
#[http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-4569 ArrayExpress Accession E-GEOD-4569]

==References==
{{RefHelp}}
<references/>

PMID:20427277

2011-07-19T16:51:40Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''McLean, S, Bowman, LA, Sanguinetti, G, Read, RC and Poole, RK''' (2010) Peroxynitrite toxicity in Escherichia coli K12 elicits expression of oxidative stress responses and protein nitration and nitrosylation.''J. Biol. Chem.'' '''285''':20724-31

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>Peroxynitrite is formed in macrophages by the diffusion-limited reaction of superoxide and nitric oxide. This highly reactive species is thought to contribute to bacterial killing by interaction with diverse targets and nitration of protein tyrosines. This work presents for the first time a comprehensive analysis of transcriptional responses to peroxynitrite under tightly controlled chemostat growth conditions. Up-regulation of the cysteine biosynthesis pathway and an increase in S-nitrosothiol levels suggest S-nitrosylation to be a consequence of peroxynitrite exposure. Genes involved in the assembly/repair of iron-sulfur clusters also show enhanced transcription. Unexpectedly, arginine biosynthesis gene transcription levels were also elevated after treatment with peroxynitrite. Analysis of the negative regulator for these genes, ArgR, showed that post-translational nitration of tyrosine residues within this protein is responsible for its degradation in vitro. Further up-regulation was seen in oxidative stress response genes, including katG and ahpCF. However, genes known to be up-regulated by nitric oxide and nitrosating agents (e.g. hmp and norVW) were unaffected. Probabilistic modeling of the transcriptomic data identified five altered transcription factors in response to peroxynitrite exposure, including OxyR and ArgR. Hydrogen peroxide can be present as a contaminant in commercially available peroxynitrite preparations. Transcriptomic analysis of cells treated with hydrogen peroxide alone also revealed up-regulation of oxidative stress response genes but not of many other genes that are up-regulated by peroxynitrite. Thus, the cellular responses to peroxynitrite and hydrogen peroxide are distinct.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=20427277 PubMed]
Online version:[http://dx.doi.org/10.1074/jbc.M109.085506 10.1074/jbc.M109.085506]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{| id="H4e00be99892f8" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.177955.H4e00be99892f8&page=177955&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
#[http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE19370 GEO Page: E-GEOD-19370]
#[http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-19370 ArrayExpress Accession E-GEOD-19370]
#[http://ech.stanford.edu/cgi-bin/search/QuerySetup.pl?resultType=Exptsets&interactive_search=yes&displayName=Escherichia%20coli%20str.%20K-12%20substr.%20MG1655&submit=Display%20Data&browseField=Transcriptional+profiling+of+E.+coli+after+addition+of+peroxynitrite+or+hydrogen+peroxide+to+aerobically+growing+cells Omics Publication E-GEOD-19370]

==References==
{{RefHelp}}
<references/>

PMID:20427277

2011-07-19T16:51:21Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''McLean, S, Bowman, LA, Sanguinetti, G, Read, RC and Poole, RK''' (2010) Peroxynitrite toxicity in Escherichia coli K12 elicits expression of oxidative stress responses and protein nitration and nitrosylation.''J. Biol. Chem.'' '''285''':20724-31

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>Peroxynitrite is formed in macrophages by the diffusion-limited reaction of superoxide and nitric oxide. This highly reactive species is thought to contribute to bacterial killing by interaction with diverse targets and nitration of protein tyrosines. This work presents for the first time a comprehensive analysis of transcriptional responses to peroxynitrite under tightly controlled chemostat growth conditions. Up-regulation of the cysteine biosynthesis pathway and an increase in S-nitrosothiol levels suggest S-nitrosylation to be a consequence of peroxynitrite exposure. Genes involved in the assembly/repair of iron-sulfur clusters also show enhanced transcription. Unexpectedly, arginine biosynthesis gene transcription levels were also elevated after treatment with peroxynitrite. Analysis of the negative regulator for these genes, ArgR, showed that post-translational nitration of tyrosine residues within this protein is responsible for its degradation in vitro. Further up-regulation was seen in oxidative stress response genes, including katG and ahpCF. However, genes known to be up-regulated by nitric oxide and nitrosating agents (e.g. hmp and norVW) were unaffected. Probabilistic modeling of the transcriptomic data identified five altered transcription factors in response to peroxynitrite exposure, including OxyR and ArgR. Hydrogen peroxide can be present as a contaminant in commercially available peroxynitrite preparations. Transcriptomic analysis of cells treated with hydrogen peroxide alone also revealed up-regulation of oxidative stress response genes but not of many other genes that are up-regulated by peroxynitrite. Thus, the cellular responses to peroxynitrite and hydrogen peroxide are distinct.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=20427277 PubMed]
Online version:[http://dx.doi.org/10.1074/jbc.M109.085506 10.1074/jbc.M109.085506]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{| id="H4e00be99892f8" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.177955.H4e00be99892f8&page=177955&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
#[http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE19370 GEO Page: E-GEOD-19370]
#[http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-19370 Accession E-GEOD-19370]
#[http://ech.stanford.edu/cgi-bin/search/QuerySetup.pl?resultType=Exptsets&interactive_search=yes&displayName=Escherichia%20coli%20str.%20K-12%20substr.%20MG1655&submit=Display%20Data&browseField=Transcriptional+profiling+of+E.+coli+after+addition+of+peroxynitrite+or+hydrogen+peroxide+to+aerobically+growing+cells Omics Publication E-GEOD-19370]

==References==
{{RefHelp}}
<references/>

PMID:19091747

2011-07-19T16:49:39Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''Davidge, KS, Sanguinetti, G, Yee, CH, Cox, AG, McLeod, CW, Monk, CE, Mann, BE, Motterlini, R and Poole, RK''' (2009) Carbon monoxide-releasing antibacterial molecules target respiration and global transcriptional regulators.''J. Biol. Chem.'' '''284''':4516-24

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>Carbon monoxide, a classical respiratory inhibitor, also exerts vasodilatory, anti-inflammatory, and antiapoptotic effects. CO-releasing molecules have therapeutic value, increasing phagocytosis and reducing sepsis-induced lethality. Here we identify for the first time the bacterial targets of Ru(CO)(3)Cl(glycinate) (CORM-3), a ruthenium-based carbonyl that liberates CO rapidly under physiological conditions. Contrary to the expectation that CO would be preferentially inhibitory at low oxygen tensions or anaerobically, Escherichia coli cultures were also sensitive to CORM-3 at concentrations equimolar with oxygen. CORM-3, assayed as ruthenium, was taken up by bacteria and rapidly delivered CO intracellularly to terminal oxidases. Microarray analysis of CORM-3-treated cells revealed extensively modified gene expression, notably down-regulation of genes encoding key aerobic respiratory complexes. Genes involved in metal metabolism, homeostasis, or transport were also differentially expressed, and free intracellular zinc levels were elevated. Probabilistic modeling of transcriptomic data identified the global transcription regulators ArcA, CRP, Fis, FNR, Fur, BaeR, CpxR, and IHF as targets and potential CO sensors. Our discovery that CORM-3 is an effective inhibitor and global regulator of gene expression, especially under aerobic conditions, has important implications for administration of CO-releasing agents in sepsis and inflammation.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=19091747 PubMed]
Online version:[http://dx.doi.org/10.1074/jbc.M808210200 10.1074/jbc.M808210200]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{| id="W4e00bc8137711" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.177954.W4e00bc8137711&page=177954&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
#[http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE12877 GEO Page: E-GEOD-12877]
#[http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE12878 GEO Page: E-GEOD-12878]
#[http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-13048 ArrayExpress Accession E-GEOD-13048]
#[http://ech.stanford.edu/cgi-bin/search/QuerySetup.pl?resultType=Exptsets&interactive_search=yes&displayName=Escherichia%20coli%20str.%20K-12%20substr.%20MG1655&submit=Display%20Data&browseField=Transcriptional+profiling+of+Escherichia+coli+after+addition+of+CORM-3+to+aerobically+growing+cells Omics Publication E-GEOD-12877]
#[http://ech.stanford.edu/cgi-bin/search/QuerySetup.pl?resultType=Exptsets&interactive_search=yes&displayName=Escherichia%20coli%20str.%20K-12%20substr.%20MG1655&submit=Display%20Data&browseField=Transcriptional+profiling+of+Escherichia+coli+after+addition+of+CO-RMs+to+anaerobically+growing+cells Omics Publication E-GEOD-21878]

==References==
{{RefHelp}}
<references/>

PMID:17189370

2011-07-19T16:42:41Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''Pullan, ST, Gidley, MD, Jones, RA, Barrett, J, Stevanin, TM, Read, RC, Green, J and Poole, RK''' (2007) Nitric oxide in chemostat-cultured Escherichia coli is sensed by Fnr and other global regulators: unaltered methionine biosynthesis indicates lack of S nitrosation.''J. Bacteriol.'' '''189''':1845-55

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>We previously elucidated the global transcriptional responses of Escherichia coli to the nitrosating agent S-nitrosoglutathione (GSNO) in both aerobic and anaerobic chemostats, demonstrated the expression of nitric oxide (NO)-protective mechanisms, and obtained evidence of critical thiol nitrosation. The present study was the first to examine the transcriptome of NO-exposed E. coli in a chemostat. Using identical conditions, we compared the GSNO stimulon with the stimulon of NO released from two NO donor compounds {3-[2-hydroxy-1-(1-methyl-ethyl)-2-nitrosohydrazino]-1-propanamine (NOC-5) and 3-(2-hydroxy-1-methyl-2-nitrosohydrazino)-N-methyl-1-propanamine (NOC-7)} simultaneously and demonstrated that there were marked differences in the transcriptional responses to these distinct nitrosative stresses. Exposure to NO did not induce met genes, suggesting that, unlike GSNO, NO does not elicit homocysteine S nitrosation and compensatory increases in methionine biosynthesis. After entry into cells, exogenous methionine provided protection from GSNO-mediated killing but not from NO-mediated killing. Anaerobic exposure to NO led to up-regulation of multiple Fnr-repressed genes and down-regulation of Fnr-activated genes, including nrfA, which encodes cytochrome c nitrite reductase, providing strong evidence that there is NO inactivation of Fnr. Other global regulators apparently affected by NO were IscR, Fur, SoxR, NsrR, and NorR. We tried to identify components of the NorR regulon by performing a microarray comparison of NO-exposed wild-type and norR mutant strains; only norVW, encoding the NO-detoxifying flavorubredoxin and its cognate reductase, were unambiguously identified. Mutation of norV or norR had no effect on E. coli survival in mouse macrophages. Thus, GSNO (a nitrosating agent) and NO have distinct cellular effects; NO more effectively interacts with global regulators that mediate adaptive responses to nitrosative stress but does not affect methionine requirements arising from homocysteine nitrosation.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=17189370 PubMed]
Online version:[http://dx.doi.org/10.1128/JB.01354-06 10.1128/JB.01354-06]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{| id="Y4dfa76180bf7b" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.177918.Y4dfa76180bf7b&page=177918&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE5075 GEO Page: E-GEOD-5075]
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE5076 GEO Page: E-GEOD-5076]
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE5137 GEO Page: E-GEOD-5137]
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE5139 GEO Page: E-GEOD-5139]
# [http://smd.stanford.edu/cgi-bin/publication/viewPublication.pl?pub_no=1034 SMD Publication]
# [http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-5098 ArrayExpress Accession: E-GEOD-5098]

==References==
{{RefHelp}}
<references/>

PMID:16804185

2011-07-19T16:26:21Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''Franchini, AG and Egli, T''' (2006) Global gene expression in Escherichia coli K-12 during short-term and long-term adaptation to glucose-limited continuous culture conditions.''Microbiology (Reading, Engl.)'' '''152''':2111-27

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>Microarray technology was used to study the cellular events that take place at the transcription level during short-term (physiological) and long-term (genetic) adaptation of the faecal indicator bacterium Escherichia coli K-12 to slow growth under limited nutrient supply. Short-term and long-term adaptation were assessed by comparing the mRNA levels isolated after 40 or 500 h of glucose-limited continuous culture at a dilution rate of 0.3 h(-1) with those from batch culture with glucose excess. A large number of genes encoding periplasmic binding proteins were upregulated, indicating that the cells are prepared for high-affinity uptake of all types of carbon sources during glucose-limited growth in continuous culture. All the genes belonging to the maltose (mal/lamB) and galactose (mgl/gal) operons were upregulated. A similar transcription pattern was observed for long-term cultures except that the expression factors were lower than in the short-term adaptation. The patterns of upregulation were confirmed by real-time RT-PCR. A switch from a fully operational citric acid cycle to the PEP-glyoxylate cycle was clearly observed in cells grown in glucose-limited continuous culture when compared to batch-grown cells and this was confirmed by transcriptome analysis. This transcriptome analysis confirms and extends the observations from previous proteome and catabolome studies in the authors' laboratory.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16804185 PubMed]
Online version:[http://dx.doi.org/10.1099/mic.0.28939-0 10.1099/mic.0.28939-0]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{| id="M4dfa7586529a3" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.177917.M4dfa7586529a3&page=177917&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE4706 GEO Page: E-GEOD-4706]
#[http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-4706 ArrayExpress Accession E-GEOD-4706]
# [http://ech.stanford.edu/cgi-bin/search/QuerySetup.pl?resultType=Exptsets&interactive_search=yes&displayName=Escherichia%20coli&submit=Display%20Data&browseField=Response+and+adaptation+to+growth+with+low+glucose+concentration Omics Publication]

==References==
{{RefHelp}}
<references/>

PMID:15647275

2011-07-19T16:22:48Z

Mdmueller: /* See also */

{{RightTOC}}

 '''Flatley, J, Barrett, J, Pullan, ST, Hughes, MN, Green, J and Poole, RK''' (2005) Transcriptional responses of Escherichia coli to S-nitrosoglutathione under defined chemostat conditions reveal major changes in methionine biosynthesis.''J. Biol. Chem.'' '''280''':10065-72

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || Nitric oxide and nitrosating agents exert powerful antimicrobial effects and are central to host defense and signal transduction. Nitric oxide and S-nitrosothiols can be metabolized by bacteria, but only a few enzymes have been shown to be important in responses to such stresses. Glycerol-limited chemostat cultures in defined medium of Escherichia coli MG1655 were used to provide bacteria in defined physiological states before applying nitrosative stress by addition of S-nitrosoglutathione (GSNO). Exposure to 200 microm GSNO for 5 min was sufficient to elicit an adaptive response as judged by the development of NO-insensitive respiration. Transcriptome profiling experiments were used to investigate the transcriptional basis of the observed adaptation to the presence of GSNO. In aerobic cultures, only 17 genes were significantly up-regulated, including genes known to be involved in NO tolerance, particularly hmp (encoding the NO-consuming flavohemoglobin Hmp) and norV (encoding flavorubredoxin). Significantly, none of the up-regulated genes were members of the Fur regulon. Six genes involved in methionine biosynthesis or regulation were significantly up-regulated; metN, metI, and metR were shown to be important for GSNO tolerance, because mutants in these genes exhibited GSNO growth sensitivity. Furthermore, exogenous methionine abrogated the toxicity of GSNO supporting the hypothesis that GSNO nitrosates homocysteine, thereby withdrawing this intermediate from the methionine biosynthetic pathway. Anaerobically, 10 genes showed significant up-regulation, of which norV, hcp, metR, and metB were also up-regulated aerobically. The data presented here reveal new genes important for nitrosative stress tolerance and demonstrate that methionine biosynthesis is a casualty of nitrosative stress.
</noinclude>
|-
|{{TableHeadingColor}} nowrap |'''Links''' || [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15647275 PubMed]
|}

==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==


{| id="Y47a9336339314" class=" tableEdit GO_table_reference"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.0.Y47a9336339314&page=0&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}


==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
# [http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-2129 ArrayExpress Accession: E-GEOD-2129]
# [http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-2095 ArrayExpress Accession: E-GEOD-2095]
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE2129 GEO Page: E-GEOD-2129]
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE2095 GEO Page: E-GEOD-2095]
# [http://ech.stanford.edu/cgi-bin/search/QuerySetup.pl?resultType=Exptsets&interactive_search=yes&displayName=Escherichia%20coli%20str.%20K-12%20substr.%20MG1655&submit=Display%20Data&browseField=Transcriptional+responses+of+Escherichia+coli+to+GSNO+under+defined+chemostat+conditions. Omics Publication: E-GEOD-2095]

==References==
{{RefHelp}}
<references/>

PMID:15647275

2011-07-19T16:21:08Z

Mdmueller: /* See also */

{{RightTOC}}

 '''Flatley, J, Barrett, J, Pullan, ST, Hughes, MN, Green, J and Poole, RK''' (2005) Transcriptional responses of Escherichia coli to S-nitrosoglutathione under defined chemostat conditions reveal major changes in methionine biosynthesis.''J. Biol. Chem.'' '''280''':10065-72

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || Nitric oxide and nitrosating agents exert powerful antimicrobial effects and are central to host defense and signal transduction. Nitric oxide and S-nitrosothiols can be metabolized by bacteria, but only a few enzymes have been shown to be important in responses to such stresses. Glycerol-limited chemostat cultures in defined medium of Escherichia coli MG1655 were used to provide bacteria in defined physiological states before applying nitrosative stress by addition of S-nitrosoglutathione (GSNO). Exposure to 200 microm GSNO for 5 min was sufficient to elicit an adaptive response as judged by the development of NO-insensitive respiration. Transcriptome profiling experiments were used to investigate the transcriptional basis of the observed adaptation to the presence of GSNO. In aerobic cultures, only 17 genes were significantly up-regulated, including genes known to be involved in NO tolerance, particularly hmp (encoding the NO-consuming flavohemoglobin Hmp) and norV (encoding flavorubredoxin). Significantly, none of the up-regulated genes were members of the Fur regulon. Six genes involved in methionine biosynthesis or regulation were significantly up-regulated; metN, metI, and metR were shown to be important for GSNO tolerance, because mutants in these genes exhibited GSNO growth sensitivity. Furthermore, exogenous methionine abrogated the toxicity of GSNO supporting the hypothesis that GSNO nitrosates homocysteine, thereby withdrawing this intermediate from the methionine biosynthetic pathway. Anaerobically, 10 genes showed significant up-regulation, of which norV, hcp, metR, and metB were also up-regulated aerobically. The data presented here reveal new genes important for nitrosative stress tolerance and demonstrate that methionine biosynthesis is a casualty of nitrosative stress.
</noinclude>
|-
|{{TableHeadingColor}} nowrap |'''Links''' || [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15647275 PubMed]
|}

==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==


{| id="Y47a9336339314" class=" tableEdit GO_table_reference"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.0.Y47a9336339314&page=0&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}


==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
# [http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-2129]
# [http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-2095]
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE2129 GEO Page: E-GEOD-2129]
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE2095 GEO Page: E-GEOD-2095]
# [http://ech.stanford.edu/cgi-bin/search/QuerySetup.pl?resultType=Exptsets&interactive_search=yes&displayName=Escherichia%20coli%20str.%20K-12%20substr.%20MG1655&submit=Display%20Data&browseField=Transcriptional+responses+of+Escherichia+coli+to+GSNO+under+defined+chemostat+conditions. Omics Publication: E-GEOD-2095]

==References==
{{RefHelp}}
<references/>

PMID:20427277

2011-07-12T16:24:53Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''McLean, S, Bowman, LA, Sanguinetti, G, Read, RC and Poole, RK''' (2010) Peroxynitrite toxicity in Escherichia coli K12 elicits expression of oxidative stress responses and protein nitration and nitrosylation.''J. Biol. Chem.'' '''285''':20724-31

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>Peroxynitrite is formed in macrophages by the diffusion-limited reaction of superoxide and nitric oxide. This highly reactive species is thought to contribute to bacterial killing by interaction with diverse targets and nitration of protein tyrosines. This work presents for the first time a comprehensive analysis of transcriptional responses to peroxynitrite under tightly controlled chemostat growth conditions. Up-regulation of the cysteine biosynthesis pathway and an increase in S-nitrosothiol levels suggest S-nitrosylation to be a consequence of peroxynitrite exposure. Genes involved in the assembly/repair of iron-sulfur clusters also show enhanced transcription. Unexpectedly, arginine biosynthesis gene transcription levels were also elevated after treatment with peroxynitrite. Analysis of the negative regulator for these genes, ArgR, showed that post-translational nitration of tyrosine residues within this protein is responsible for its degradation in vitro. Further up-regulation was seen in oxidative stress response genes, including katG and ahpCF. However, genes known to be up-regulated by nitric oxide and nitrosating agents (e.g. hmp and norVW) were unaffected. Probabilistic modeling of the transcriptomic data identified five altered transcription factors in response to peroxynitrite exposure, including OxyR and ArgR. Hydrogen peroxide can be present as a contaminant in commercially available peroxynitrite preparations. Transcriptomic analysis of cells treated with hydrogen peroxide alone also revealed up-regulation of oxidative stress response genes but not of many other genes that are up-regulated by peroxynitrite. Thus, the cellular responses to peroxynitrite and hydrogen peroxide are distinct.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=20427277 PubMed]
Online version:[http://dx.doi.org/10.1074/jbc.M109.085506 10.1074/jbc.M109.085506]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{| id="H4e00be99892f8" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.177955.H4e00be99892f8&page=177955&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
#[http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE19370 GEO Page: E-GEOD-19370]
#[http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-GEOD-19370&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession E-GEOD-19370]
#[http://ech.stanford.edu/cgi-bin/search/QuerySetup.pl?resultType=Exptsets&interactive_search=yes&displayName=Escherichia%20coli%20str.%20K-12%20substr.%20MG1655&submit=Display%20Data&browseField=Transcriptional+profiling+of+E.+coli+after+addition+of+peroxynitrite+or+hydrogen+peroxide+to+aerobically+growing+cells Omics Publication E-GEOD-19370]

==References==
{{RefHelp}}
<references/>

PMID:19091747

2011-07-12T16:22:32Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''Davidge, KS, Sanguinetti, G, Yee, CH, Cox, AG, McLeod, CW, Monk, CE, Mann, BE, Motterlini, R and Poole, RK''' (2009) Carbon monoxide-releasing antibacterial molecules target respiration and global transcriptional regulators.''J. Biol. Chem.'' '''284''':4516-24

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>Carbon monoxide, a classical respiratory inhibitor, also exerts vasodilatory, anti-inflammatory, and antiapoptotic effects. CO-releasing molecules have therapeutic value, increasing phagocytosis and reducing sepsis-induced lethality. Here we identify for the first time the bacterial targets of Ru(CO)(3)Cl(glycinate) (CORM-3), a ruthenium-based carbonyl that liberates CO rapidly under physiological conditions. Contrary to the expectation that CO would be preferentially inhibitory at low oxygen tensions or anaerobically, Escherichia coli cultures were also sensitive to CORM-3 at concentrations equimolar with oxygen. CORM-3, assayed as ruthenium, was taken up by bacteria and rapidly delivered CO intracellularly to terminal oxidases. Microarray analysis of CORM-3-treated cells revealed extensively modified gene expression, notably down-regulation of genes encoding key aerobic respiratory complexes. Genes involved in metal metabolism, homeostasis, or transport were also differentially expressed, and free intracellular zinc levels were elevated. Probabilistic modeling of transcriptomic data identified the global transcription regulators ArcA, CRP, Fis, FNR, Fur, BaeR, CpxR, and IHF as targets and potential CO sensors. Our discovery that CORM-3 is an effective inhibitor and global regulator of gene expression, especially under aerobic conditions, has important implications for administration of CO-releasing agents in sepsis and inflammation.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=19091747 PubMed]
Online version:[http://dx.doi.org/10.1074/jbc.M808210200 10.1074/jbc.M808210200]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{| id="W4e00bc8137711" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.177954.W4e00bc8137711&page=177954&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
#[http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE12877 GEO Page: E-GEOD-12877]
#[http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE12878 GEO Page: E-GEOD-12878]
#[http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-GEOD-13048&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession E-GEOD-13048]
#[http://ech.stanford.edu/cgi-bin/search/QuerySetup.pl?resultType=Exptsets&interactive_search=yes&displayName=Escherichia%20coli%20str.%20K-12%20substr.%20MG1655&submit=Display%20Data&browseField=Transcriptional+profiling+of+Escherichia+coli+after+addition+of+CORM-3+to+aerobically+growing+cells Omics Publication E-GEOD-12877]
#[http://ech.stanford.edu/cgi-bin/search/QuerySetup.pl?resultType=Exptsets&interactive_search=yes&displayName=Escherichia%20coli%20str.%20K-12%20substr.%20MG1655&submit=Display%20Data&browseField=Transcriptional+profiling+of+Escherichia+coli+after+addition+of+CO-RMs+to+anaerobically+growing+cells Omics Publication E-GEOD-21878]

==References==
{{RefHelp}}
<references/>

PMID:16804185

2011-07-12T15:49:54Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''Franchini, AG and Egli, T''' (2006) Global gene expression in Escherichia coli K-12 during short-term and long-term adaptation to glucose-limited continuous culture conditions.''Microbiology (Reading, Engl.)'' '''152''':2111-27

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>Microarray technology was used to study the cellular events that take place at the transcription level during short-term (physiological) and long-term (genetic) adaptation of the faecal indicator bacterium Escherichia coli K-12 to slow growth under limited nutrient supply. Short-term and long-term adaptation were assessed by comparing the mRNA levels isolated after 40 or 500 h of glucose-limited continuous culture at a dilution rate of 0.3 h(-1) with those from batch culture with glucose excess. A large number of genes encoding periplasmic binding proteins were upregulated, indicating that the cells are prepared for high-affinity uptake of all types of carbon sources during glucose-limited growth in continuous culture. All the genes belonging to the maltose (mal/lamB) and galactose (mgl/gal) operons were upregulated. A similar transcription pattern was observed for long-term cultures except that the expression factors were lower than in the short-term adaptation. The patterns of upregulation were confirmed by real-time RT-PCR. A switch from a fully operational citric acid cycle to the PEP-glyoxylate cycle was clearly observed in cells grown in glucose-limited continuous culture when compared to batch-grown cells and this was confirmed by transcriptome analysis. This transcriptome analysis confirms and extends the observations from previous proteome and catabolome studies in the authors' laboratory.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16804185 PubMed]
Online version:[http://dx.doi.org/10.1099/mic.0.28939-0 10.1099/mic.0.28939-0]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{| id="M4dfa7586529a3" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.177917.M4dfa7586529a3&page=177917&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE4706 GEO Page: E-GEOD-4706]
#[http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-GEOD-4706&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession E-GEOD-4706]
# [http://ech.stanford.edu/cgi-bin/search/QuerySetup.pl?resultType=Exptsets&interactive_search=yes&displayName=Escherichia%20coli&submit=Display%20Data&browseField=Response+and+adaptation+to+growth+with+low+glucose+concentration Omics Publication]

==References==
{{RefHelp}}
<references/>

PMID:15647275

2011-07-12T15:38:01Z

Mdmueller: /* See also */

{{RightTOC}}

 '''Flatley, J, Barrett, J, Pullan, ST, Hughes, MN, Green, J and Poole, RK''' (2005) Transcriptional responses of Escherichia coli to S-nitrosoglutathione under defined chemostat conditions reveal major changes in methionine biosynthesis.''J. Biol. Chem.'' '''280''':10065-72

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || Nitric oxide and nitrosating agents exert powerful antimicrobial effects and are central to host defense and signal transduction. Nitric oxide and S-nitrosothiols can be metabolized by bacteria, but only a few enzymes have been shown to be important in responses to such stresses. Glycerol-limited chemostat cultures in defined medium of Escherichia coli MG1655 were used to provide bacteria in defined physiological states before applying nitrosative stress by addition of S-nitrosoglutathione (GSNO). Exposure to 200 microm GSNO for 5 min was sufficient to elicit an adaptive response as judged by the development of NO-insensitive respiration. Transcriptome profiling experiments were used to investigate the transcriptional basis of the observed adaptation to the presence of GSNO. In aerobic cultures, only 17 genes were significantly up-regulated, including genes known to be involved in NO tolerance, particularly hmp (encoding the NO-consuming flavohemoglobin Hmp) and norV (encoding flavorubredoxin). Significantly, none of the up-regulated genes were members of the Fur regulon. Six genes involved in methionine biosynthesis or regulation were significantly up-regulated; metN, metI, and metR were shown to be important for GSNO tolerance, because mutants in these genes exhibited GSNO growth sensitivity. Furthermore, exogenous methionine abrogated the toxicity of GSNO supporting the hypothesis that GSNO nitrosates homocysteine, thereby withdrawing this intermediate from the methionine biosynthetic pathway. Anaerobically, 10 genes showed significant up-regulation, of which norV, hcp, metR, and metB were also up-regulated aerobically. The data presented here reveal new genes important for nitrosative stress tolerance and demonstrate that methionine biosynthesis is a casualty of nitrosative stress.
</noinclude>
|-
|{{TableHeadingColor}} nowrap |'''Links''' || [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15647275 PubMed]
|}

==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==


{| id="Y47a9336339314" class=" tableEdit GO_table_reference"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.0.Y47a9336339314&page=0&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}


==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
# [http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-GEOD-2129&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession E-GEOD-2129]
# [http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-GEOD-2095&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession E-GEOD-2095]
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE2129 GEO Page: E-GEOD-2129]
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE2095 GEO Page: E-GEOD-2095]
# [http://ech.stanford.edu/cgi-bin/search/QuerySetup.pl?resultType=Exptsets&interactive_search=yes&displayName=Escherichia%20coli%20str.%20K-12%20substr.%20MG1655&submit=Display%20Data&browseField=Transcriptional+responses+of+Escherichia+coli+to+GSNO+under+defined+chemostat+conditions. Omics Publication: E-GEOD-2095]

==References==
{{RefHelp}}
<references/>

PMID:15647275

2011-07-12T15:36:18Z

Mdmueller: /* See also */

{{RightTOC}}

 '''Flatley, J, Barrett, J, Pullan, ST, Hughes, MN, Green, J and Poole, RK''' (2005) Transcriptional responses of Escherichia coli to S-nitrosoglutathione under defined chemostat conditions reveal major changes in methionine biosynthesis.''J. Biol. Chem.'' '''280''':10065-72

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || Nitric oxide and nitrosating agents exert powerful antimicrobial effects and are central to host defense and signal transduction. Nitric oxide and S-nitrosothiols can be metabolized by bacteria, but only a few enzymes have been shown to be important in responses to such stresses. Glycerol-limited chemostat cultures in defined medium of Escherichia coli MG1655 were used to provide bacteria in defined physiological states before applying nitrosative stress by addition of S-nitrosoglutathione (GSNO). Exposure to 200 microm GSNO for 5 min was sufficient to elicit an adaptive response as judged by the development of NO-insensitive respiration. Transcriptome profiling experiments were used to investigate the transcriptional basis of the observed adaptation to the presence of GSNO. In aerobic cultures, only 17 genes were significantly up-regulated, including genes known to be involved in NO tolerance, particularly hmp (encoding the NO-consuming flavohemoglobin Hmp) and norV (encoding flavorubredoxin). Significantly, none of the up-regulated genes were members of the Fur regulon. Six genes involved in methionine biosynthesis or regulation were significantly up-regulated; metN, metI, and metR were shown to be important for GSNO tolerance, because mutants in these genes exhibited GSNO growth sensitivity. Furthermore, exogenous methionine abrogated the toxicity of GSNO supporting the hypothesis that GSNO nitrosates homocysteine, thereby withdrawing this intermediate from the methionine biosynthetic pathway. Anaerobically, 10 genes showed significant up-regulation, of which norV, hcp, metR, and metB were also up-regulated aerobically. The data presented here reveal new genes important for nitrosative stress tolerance and demonstrate that methionine biosynthesis is a casualty of nitrosative stress.
</noinclude>
|-
|{{TableHeadingColor}} nowrap |'''Links''' || [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15647275 PubMed]
|}

==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==


{| id="Y47a9336339314" class=" tableEdit GO_table_reference"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.0.Y47a9336339314&page=0&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}


==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
# [http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-GEOD-2129&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession E-GEOD-2129]
# [http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-GEOD-2095&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession E-GEOD-2095]
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE2129 GEO Page: E-GEOD-2129]
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE2095 GEO Page: E-GEOD-2095]
# [http://ech.stanford.edu/publication.shtml?q=* Omics Publication]

==References==
{{RefHelp}}
<references/>

PMID:15647275

2011-07-12T15:33:18Z

Mdmueller: /* See also */

{{RightTOC}}

 '''Flatley, J, Barrett, J, Pullan, ST, Hughes, MN, Green, J and Poole, RK''' (2005) Transcriptional responses of Escherichia coli to S-nitrosoglutathione under defined chemostat conditions reveal major changes in methionine biosynthesis.''J. Biol. Chem.'' '''280''':10065-72

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || Nitric oxide and nitrosating agents exert powerful antimicrobial effects and are central to host defense and signal transduction. Nitric oxide and S-nitrosothiols can be metabolized by bacteria, but only a few enzymes have been shown to be important in responses to such stresses. Glycerol-limited chemostat cultures in defined medium of Escherichia coli MG1655 were used to provide bacteria in defined physiological states before applying nitrosative stress by addition of S-nitrosoglutathione (GSNO). Exposure to 200 microm GSNO for 5 min was sufficient to elicit an adaptive response as judged by the development of NO-insensitive respiration. Transcriptome profiling experiments were used to investigate the transcriptional basis of the observed adaptation to the presence of GSNO. In aerobic cultures, only 17 genes were significantly up-regulated, including genes known to be involved in NO tolerance, particularly hmp (encoding the NO-consuming flavohemoglobin Hmp) and norV (encoding flavorubredoxin). Significantly, none of the up-regulated genes were members of the Fur regulon. Six genes involved in methionine biosynthesis or regulation were significantly up-regulated; metN, metI, and metR were shown to be important for GSNO tolerance, because mutants in these genes exhibited GSNO growth sensitivity. Furthermore, exogenous methionine abrogated the toxicity of GSNO supporting the hypothesis that GSNO nitrosates homocysteine, thereby withdrawing this intermediate from the methionine biosynthetic pathway. Anaerobically, 10 genes showed significant up-regulation, of which norV, hcp, metR, and metB were also up-regulated aerobically. The data presented here reveal new genes important for nitrosative stress tolerance and demonstrate that methionine biosynthesis is a casualty of nitrosative stress.
</noinclude>
|-
|{{TableHeadingColor}} nowrap |'''Links''' || [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15647275 PubMed]
|}

==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==


{| id="Y47a9336339314" class=" tableEdit GO_table_reference"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.0.Y47a9336339314&page=0&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}


==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
# [http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-GEOD-2129&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession E-GEOD-2129]
# [http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-GEOD-2095&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession E-GEOD-2095]
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE2129 GEO Page: E-GEOD-2129]
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE2095 GEO Page: E-GEOD-2095]
# [http://ech.stanford.edu/cgi-bin/search/QuerySetup.pl?resultType=Exptsets&interactive_search=yes&displayName=Escherichia%20coli%20str.%20K-12%20substr.%20MG1655&submit=Display%20Data&browseField=Transcriptional+responses+of+Escherichia+coli+to+GSNO+under+defined+chemostat+conditions. Omics Publication]

==References==
{{RefHelp}}
<references/>

PMID:16804185

2011-06-28T19:11:53Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''Franchini, AG and Egli, T''' (2006) Global gene expression in Escherichia coli K-12 during short-term and long-term adaptation to glucose-limited continuous culture conditions.''Microbiology (Reading, Engl.)'' '''152''':2111-27

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>Microarray technology was used to study the cellular events that take place at the transcription level during short-term (physiological) and long-term (genetic) adaptation of the faecal indicator bacterium Escherichia coli K-12 to slow growth under limited nutrient supply. Short-term and long-term adaptation were assessed by comparing the mRNA levels isolated after 40 or 500 h of glucose-limited continuous culture at a dilution rate of 0.3 h(-1) with those from batch culture with glucose excess. A large number of genes encoding periplasmic binding proteins were upregulated, indicating that the cells are prepared for high-affinity uptake of all types of carbon sources during glucose-limited growth in continuous culture. All the genes belonging to the maltose (mal/lamB) and galactose (mgl/gal) operons were upregulated. A similar transcription pattern was observed for long-term cultures except that the expression factors were lower than in the short-term adaptation. The patterns of upregulation were confirmed by real-time RT-PCR. A switch from a fully operational citric acid cycle to the PEP-glyoxylate cycle was clearly observed in cells grown in glucose-limited continuous culture when compared to batch-grown cells and this was confirmed by transcriptome analysis. This transcriptome analysis confirms and extends the observations from previous proteome and catabolome studies in the authors' laboratory.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16804185 PubMed]
Online version:[http://dx.doi.org/10.1099/mic.0.28939-0 10.1099/mic.0.28939-0]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{| id="M4dfa7586529a3" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.177917.M4dfa7586529a3&page=177917&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE4706 GEO Page: E-GEOD-4706]
#[http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-GEOD-4706&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession E-GEOD-4706]
# [http://smd.stanford.edu/cgi-bin/publication/viewPublication.pl?pub_no=1035 SMD Publication]

==References==
{{RefHelp}}
<references/>

PMID:19091747

2011-06-28T19:09:26Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''Davidge, KS, Sanguinetti, G, Yee, CH, Cox, AG, McLeod, CW, Monk, CE, Mann, BE, Motterlini, R and Poole, RK''' (2009) Carbon monoxide-releasing antibacterial molecules target respiration and global transcriptional regulators.''J. Biol. Chem.'' '''284''':4516-24

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>Carbon monoxide, a classical respiratory inhibitor, also exerts vasodilatory, anti-inflammatory, and antiapoptotic effects. CO-releasing molecules have therapeutic value, increasing phagocytosis and reducing sepsis-induced lethality. Here we identify for the first time the bacterial targets of Ru(CO)(3)Cl(glycinate) (CORM-3), a ruthenium-based carbonyl that liberates CO rapidly under physiological conditions. Contrary to the expectation that CO would be preferentially inhibitory at low oxygen tensions or anaerobically, Escherichia coli cultures were also sensitive to CORM-3 at concentrations equimolar with oxygen. CORM-3, assayed as ruthenium, was taken up by bacteria and rapidly delivered CO intracellularly to terminal oxidases. Microarray analysis of CORM-3-treated cells revealed extensively modified gene expression, notably down-regulation of genes encoding key aerobic respiratory complexes. Genes involved in metal metabolism, homeostasis, or transport were also differentially expressed, and free intracellular zinc levels were elevated. Probabilistic modeling of transcriptomic data identified the global transcription regulators ArcA, CRP, Fis, FNR, Fur, BaeR, CpxR, and IHF as targets and potential CO sensors. Our discovery that CORM-3 is an effective inhibitor and global regulator of gene expression, especially under aerobic conditions, has important implications for administration of CO-releasing agents in sepsis and inflammation.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=19091747 PubMed]
Online version:[http://dx.doi.org/10.1074/jbc.M808210200 10.1074/jbc.M808210200]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{| id="W4e00bc8137711" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.177954.W4e00bc8137711&page=177954&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
#[http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE12877 GEO Page: E-GEOD-12877]
#[http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE12878 GEO Page: E-GEOD-12878]
#[http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-GEOD-13048&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession E-GEOD-13048]
#[http://smd.stanford.edu/cgi-bin/publication/viewPublication.pl?pub_no=1036 SMD Publication]

==References==
{{RefHelp}}
<references/>

PMID:19091747

2011-06-28T19:09:03Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''Davidge, KS, Sanguinetti, G, Yee, CH, Cox, AG, McLeod, CW, Monk, CE, Mann, BE, Motterlini, R and Poole, RK''' (2009) Carbon monoxide-releasing antibacterial molecules target respiration and global transcriptional regulators.''J. Biol. Chem.'' '''284''':4516-24

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>Carbon monoxide, a classical respiratory inhibitor, also exerts vasodilatory, anti-inflammatory, and antiapoptotic effects. CO-releasing molecules have therapeutic value, increasing phagocytosis and reducing sepsis-induced lethality. Here we identify for the first time the bacterial targets of Ru(CO)(3)Cl(glycinate) (CORM-3), a ruthenium-based carbonyl that liberates CO rapidly under physiological conditions. Contrary to the expectation that CO would be preferentially inhibitory at low oxygen tensions or anaerobically, Escherichia coli cultures were also sensitive to CORM-3 at concentrations equimolar with oxygen. CORM-3, assayed as ruthenium, was taken up by bacteria and rapidly delivered CO intracellularly to terminal oxidases. Microarray analysis of CORM-3-treated cells revealed extensively modified gene expression, notably down-regulation of genes encoding key aerobic respiratory complexes. Genes involved in metal metabolism, homeostasis, or transport were also differentially expressed, and free intracellular zinc levels were elevated. Probabilistic modeling of transcriptomic data identified the global transcription regulators ArcA, CRP, Fis, FNR, Fur, BaeR, CpxR, and IHF as targets and potential CO sensors. Our discovery that CORM-3 is an effective inhibitor and global regulator of gene expression, especially under aerobic conditions, has important implications for administration of CO-releasing agents in sepsis and inflammation.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=19091747 PubMed]
Online version:[http://dx.doi.org/10.1074/jbc.M808210200 10.1074/jbc.M808210200]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{| id="W4e00bc8137711" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.177954.W4e00bc8137711&page=177954&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
#[http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE12877 GEO Page: E-GEOD-12877]
#[http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE12878 GEO Page: E-GEOD-12878]
#[http://smd.stanford.edu/cgi-bin/publication/viewPublication.pl?pub_no=1036 SMD Publication]
#[http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-GEOD-13048&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession E-GEOD-13048]

==References==
{{RefHelp}}
<references/>

PMID:20427277

2011-06-28T19:06:06Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''McLean, S, Bowman, LA, Sanguinetti, G, Read, RC and Poole, RK''' (2010) Peroxynitrite toxicity in Escherichia coli K12 elicits expression of oxidative stress responses and protein nitration and nitrosylation.''J. Biol. Chem.'' '''285''':20724-31

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>Peroxynitrite is formed in macrophages by the diffusion-limited reaction of superoxide and nitric oxide. This highly reactive species is thought to contribute to bacterial killing by interaction with diverse targets and nitration of protein tyrosines. This work presents for the first time a comprehensive analysis of transcriptional responses to peroxynitrite under tightly controlled chemostat growth conditions. Up-regulation of the cysteine biosynthesis pathway and an increase in S-nitrosothiol levels suggest S-nitrosylation to be a consequence of peroxynitrite exposure. Genes involved in the assembly/repair of iron-sulfur clusters also show enhanced transcription. Unexpectedly, arginine biosynthesis gene transcription levels were also elevated after treatment with peroxynitrite. Analysis of the negative regulator for these genes, ArgR, showed that post-translational nitration of tyrosine residues within this protein is responsible for its degradation in vitro. Further up-regulation was seen in oxidative stress response genes, including katG and ahpCF. However, genes known to be up-regulated by nitric oxide and nitrosating agents (e.g. hmp and norVW) were unaffected. Probabilistic modeling of the transcriptomic data identified five altered transcription factors in response to peroxynitrite exposure, including OxyR and ArgR. Hydrogen peroxide can be present as a contaminant in commercially available peroxynitrite preparations. Transcriptomic analysis of cells treated with hydrogen peroxide alone also revealed up-regulation of oxidative stress response genes but not of many other genes that are up-regulated by peroxynitrite. Thus, the cellular responses to peroxynitrite and hydrogen peroxide are distinct.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=20427277 PubMed]
Online version:[http://dx.doi.org/10.1074/jbc.M109.085506 10.1074/jbc.M109.085506]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{| id="H4e00be99892f8" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.177955.H4e00be99892f8&page=177955&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
#[http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE19370 GEO Page: E-GEOD-19370]
#[http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-GEOD-19370&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession E-GEOD-19370]
#[http://smd.stanford.edu/cgi-bin/publication/viewPublication.pl?pub_no=1041 SMD Publication]

==References==
{{RefHelp}}
<references/>

PMID:15647275

2011-06-28T19:04:24Z

Mdmueller: /* See also */

{{RightTOC}}

 '''Flatley, J, Barrett, J, Pullan, ST, Hughes, MN, Green, J and Poole, RK''' (2005) Transcriptional responses of Escherichia coli to S-nitrosoglutathione under defined chemostat conditions reveal major changes in methionine biosynthesis.''J. Biol. Chem.'' '''280''':10065-72

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || Nitric oxide and nitrosating agents exert powerful antimicrobial effects and are central to host defense and signal transduction. Nitric oxide and S-nitrosothiols can be metabolized by bacteria, but only a few enzymes have been shown to be important in responses to such stresses. Glycerol-limited chemostat cultures in defined medium of Escherichia coli MG1655 were used to provide bacteria in defined physiological states before applying nitrosative stress by addition of S-nitrosoglutathione (GSNO). Exposure to 200 microm GSNO for 5 min was sufficient to elicit an adaptive response as judged by the development of NO-insensitive respiration. Transcriptome profiling experiments were used to investigate the transcriptional basis of the observed adaptation to the presence of GSNO. In aerobic cultures, only 17 genes were significantly up-regulated, including genes known to be involved in NO tolerance, particularly hmp (encoding the NO-consuming flavohemoglobin Hmp) and norV (encoding flavorubredoxin). Significantly, none of the up-regulated genes were members of the Fur regulon. Six genes involved in methionine biosynthesis or regulation were significantly up-regulated; metN, metI, and metR were shown to be important for GSNO tolerance, because mutants in these genes exhibited GSNO growth sensitivity. Furthermore, exogenous methionine abrogated the toxicity of GSNO supporting the hypothesis that GSNO nitrosates homocysteine, thereby withdrawing this intermediate from the methionine biosynthetic pathway. Anaerobically, 10 genes showed significant up-regulation, of which norV, hcp, metR, and metB were also up-regulated aerobically. The data presented here reveal new genes important for nitrosative stress tolerance and demonstrate that methionine biosynthesis is a casualty of nitrosative stress.
</noinclude>
|-
|{{TableHeadingColor}} nowrap |'''Links''' || [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15647275 PubMed]
|}

==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==


{| id="Y47a9336339314" class=" tableEdit GO_table_reference"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.0.Y47a9336339314&page=0&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}


==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
# [http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-GEOD-2129&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession E-GEOD-2129]
# [http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-GEOD-2095&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession E-GEOD-2095]
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE2129 GEO Page: E-GEOD-2129]
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE2095 GEO Page: E-GEOD-2095]
# [http://smd.stanford.edu/cgi-bin/publication/viewPublication.pl?pub_no=1037 SMD Publication]

==References==
{{RefHelp}}
<references/>

PMID:16913923

2011-06-28T18:56:14Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''Berney, M, Weilenmann, HU and Egli, T''' (2006) Gene expression of Escherichia coli in continuous culture during adaptation to artificial sunlight.''Environ. Microbiol.'' '''8''':1635-47

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>Escherichia coli growing in continuous culture under continuous UVA irradiation exhibits growth inhibition with a subsequent adaptation to the stress. Transcriptome analysis was performed during transient growth inhibition and in the UVA light-adapted growth state. The results indicate that UVA light induces stringent response and an additional response that includes the upregulation of the synthesis of valine, isoleucine, leucine, phenylalanine, histidine and glutamate. The induction of several SOS response-genes strongly points to DNA damage as a result of UVA exposure. The involvement of oxidative stress was observed with the induction of ahpCF. Taken together it supports the hypothesis of the production of reactive oxygen species by UVA light. In the UVA-adapted cell population strong repression of the acid tolerance response was found. We identified the enzyme chorismate mutase as a possible chromophore for UVA light-inactivation and found strong repression of the pyrBI operon and the gene mgtA encoding for an ATP-dependent Mg2+ transporter. Furthermore, our results indicate that the role of RpoS may not be as important in the adaptation of E. coli to UVA light as it was implicated by previous results with starved cells, but that RpoS might be of crucial importance for the resistance under transient light exposure.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16913923 PubMed]
Online version:[http://dx.doi.org/10.1111/j.1462-2920.2006.01057.x 10.1111/j.1462-2920.2006.01057.x]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{| id="J4e00c153e967b" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.177956.J4e00c153e967b&page=177956&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
#[http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE4569 GEO Page: E-GEOD-4569]
#[http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-GEOD-4569&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession E-GEOD-4569]

==References==
{{RefHelp}}
<references/>

PMID:17600050

2011-06-28T18:54:39Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''Ihssen, J, Grasselli, E, Bassin, C, François, P, Piffaretti, JC, Köster, W, Schrenzel, J and Egli, T''' (2007) Comparative genomic hybridization and physiological characterization of environmental isolates indicate that significant (eco-)physiological properties are highly conserved in the species Escherichia coli.''Microbiology (Reading, Engl.)'' '''153''':2052-66

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>Escherichia coli, the common inhabitant of the mammalian intestine, exhibits considerable intraspecies genomic variation, which has been suggested to reflect adaptation to different ecological niches. Also, regulatory trade-offs, e.g. between catabolic versatility and stress protection, are thought to result in significant physiological differences between strains. For these reasons, the relevance of experimental observations made for 'domesticated' E. coli strains with regard to the behaviour of this species in its natural environments is often questioned and doubts are frequently raised on the status of E. coli as a defined species. The variability of important (eco-)physiological functions, such as carbon substrate uptake and breakdown capabilities, as well as stress defence mechanisms, in the genomes of commensal and pathogenic E. coli strains were therefore investigated. Furthermore, (eco-)physiological properties of environmental strains were compared to standard laboratory strain K-12 MG1655. Catabolic, stress protection, and carbon- and energy source transport operons showed a very low intraspecies variability in 57 commensal and pathogenic E. coli. Environmental isolates adapted to glucose-limited growth in a similar way as E. coli MG1655, namely by increasing their catabolic flexibility and by inducing high-affinity substrate uptake systems. The results obtained indicate that significant (eco-)physiological properties are highly conserved in the natural population of E. coli. This questions the proposed dominant role of horizontal gene transfer for niche adaptation.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=17600050 PubMed]
Online version:[http://dx.doi.org/10.1099/mic.0.2006/002006-0 10.1099/mic.0.2006/002006-0]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{| id="B4e00c27d75023" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.177957.B4e00c27d75023&page=177957&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE6407 GEO Page: E-GEOD-6407]
# [http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-GEOD-6407&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession E-GEOD-6407]

==References==
{{RefHelp}}
<references/>

PMID:15659689

2011-06-28T18:50:31Z

Mdmueller: /* See Also */

{{RightTOC}}

 '''Lee, LJ, Barrett, JA and Poole, RK''' (2005) Genome-wide transcriptional response of chemostat-cultured Escherichia coli to zinc.''J. Bacteriol.'' '''187''':1124-34

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || Zinc is an essential trace metal ion for growth, but an excess of Zn is toxic and microorganisms express diverse resistance mechanisms. To understand global bacterial responses to excess Zn, we conducted transcriptome profiling experiments comparing Escherichia coli MG1655 grown under control conditions and cells grown with a toxic, sublethal ZnSO4 concentration (0.2 mM). Cultures were grown in a defined medium lacking inorganic phosphate, permitting maximum Zn bioavailability, and in glycerol-limited chemostats at a constant growth rate and pH. Sixty-four genes were significantly up-regulated by Zn stress, including genes known to be involved in Zn tolerance, particularly zntA, zraP, and hydG. Microarray transcriptome profiling was confirmed by real-time PCR determinations of cusF (involved in Ag and Cu efflux), ais (an Al-inducible gene), asr (encoding an acid shock-inducible periplasmic protein), cpxP (a periplasmic chaperone gene), and basR. Five up-regulated genes, basR and basS [encoding a sensor-regulator implicated in Salmonella in Fe(III) sensing and antibiotic resistance], fliM (flagellar synthesis), and ycdM and yibD (both with unknown functions), are important for growth resistance to zinc, since mutants with mutations in these genes exhibited zinc sensitivity in liquid media and on metal gradient plates. Fifty-eight genes were significantly down-regulated by Zn stress; notably, several of these genes were involved in protection against acid stress. Since the mdt operon (encoding a multidrug resistance pump) was also up-regulated, these findings have important implications for understanding not only Zn homeostasis but also how bacterial antibiotic resistance is modulated by metal ions.
</noinclude>
|-
|{{TableHeadingColor}} nowrap |'''Links''' || [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15659689 PubMed]
|}

==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==


{| id="F47ab8af78a860" class=" tableEdit GO_table_reference"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.0.F47ab8af78a860&page=0&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}


==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See Also==
# [http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-MEXP-222&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession E-MEXP-222]

==References==
{{RefHelp}}
<references/>

PMID:16799466

2011-06-28T18:49:57Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''Blot, N, Mavathur, R, Geertz, M, Travers, A and Muskhelishvili, G''' (2006) Homeostatic regulation of supercoiling sensitivity coordinates transcription of the bacterial genome.''EMBO Rep.'' '''7''':710-5

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>Regulation of cellular growth implies spatiotemporally coordinated programmes of gene transcription. A central question, therefore, is how global transcription is coordinated in the genome. The growth of the unicellular organism Escherichia coli is associated with changes in both the global superhelicity modulated by cellular topoisomerase activity and the relative proportions of the abundant DNA-architectural chromatin proteins. Using a DNA-microarray-based approach that combines mutations in the genes of two important chromatin proteins with induced changes of DNA superhelicity, we demonstrate that genomic transcription is tightly associated with the spatial distribution of supercoiling sensitivity, which in turn depends on chromatin proteins. We further demonstrate that essential metabolic pathways involved in the maintenance of growth respond distinctly to changes of superhelicity. We infer that a homeostatic mechanism organizing the supercoiling sensitivity is coordinating the growth-phase-dependent transcription of the genome.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16799466 PubMed]
Online version:[http://dx.doi.org/10.1038/sj.embor.7400729 10.1038/sj.embor.7400729]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{| id="U4e00c7c5d178e" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.177958.U4e00c7c5d178e&page=177958&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
# [http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-MEXP-462&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession E-MEXP-462]
# [http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-MEXP-464&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession E-MEXP-464]
# [http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-MEXP-465&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession E-MEXP-465]

==References==
{{RefHelp}}
<references/>

PMID:21695201

2011-06-28T18:46:10Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''Murata, M, Fujimoto, H, Nishimura, K, Charoensuk, K, Nagamitsu, H, Raina, S, Kosaka, T, Oshima, T, Ogasawara, N and Yamada, M''' (2011) Molecular Strategy for Survival at a Critical High Temperature in Eschierichia coli.''PLoS ONE'' '''6''':e20063

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>The molecular mechanism supporting survival at a critical high temperature (CHT) in Escherichia coli was investigated. Genome-wide screening with a single-gene knockout library provided a list of genes indispensable for growth at 47°C, called thermotolerant genes. Genes for which expression was affected by exposure to CHT were identified by DNA chip analysis. Unexpectedly, the former contents did not overlap with the latter except for dnaJ and dnaK, indicating that a specific set of non-heat shock genes is required for the organism to survive under such a severe condition. More than half of the mutants of the thermotolerant genes were found to be sensitive to H(2)O(2) at 30°C, suggesting that the mechanism of thermotolerance partially overlaps with that of oxidative stress resistance. Their encoded enzymes or proteins are related to outer membrane organization, DNA double-strand break repair, tRNA modification, protein quality control, translation control or cell division. DNA chip analyses of essential genes suggest that many of the genes encoding ribosomal proteins are down-regulated at CHT. Bioinformatics analysis and comparison with the genomic information of other microbes suggest that E. coli possesses several systems for survival at CHT. This analysis allows us to speculate that a lipopolysaccharide biosynthesis system for outer membrane organization and a sulfur-relay system for tRNA modification have been acquired by horizontal gene transfer.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=21695201 PubMed]
Online version:[http://dx.doi.org/10.1371/journal.pone.0020063 10.1371/journal.pone.0020063]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{| id="O4e03724037c15" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.177984.O4e03724037c15&page=177984&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==

# [http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-MEXP-3191&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession E-MEXP-3191]

==References==
{{RefHelp}}
<references/>

PMID:17189370

2011-06-28T18:45:16Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''Pullan, ST, Gidley, MD, Jones, RA, Barrett, J, Stevanin, TM, Read, RC, Green, J and Poole, RK''' (2007) Nitric oxide in chemostat-cultured Escherichia coli is sensed by Fnr and other global regulators: unaltered methionine biosynthesis indicates lack of S nitrosation.''J. Bacteriol.'' '''189''':1845-55

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>We previously elucidated the global transcriptional responses of Escherichia coli to the nitrosating agent S-nitrosoglutathione (GSNO) in both aerobic and anaerobic chemostats, demonstrated the expression of nitric oxide (NO)-protective mechanisms, and obtained evidence of critical thiol nitrosation. The present study was the first to examine the transcriptome of NO-exposed E. coli in a chemostat. Using identical conditions, we compared the GSNO stimulon with the stimulon of NO released from two NO donor compounds {3-[2-hydroxy-1-(1-methyl-ethyl)-2-nitrosohydrazino]-1-propanamine (NOC-5) and 3-(2-hydroxy-1-methyl-2-nitrosohydrazino)-N-methyl-1-propanamine (NOC-7)} simultaneously and demonstrated that there were marked differences in the transcriptional responses to these distinct nitrosative stresses. Exposure to NO did not induce met genes, suggesting that, unlike GSNO, NO does not elicit homocysteine S nitrosation and compensatory increases in methionine biosynthesis. After entry into cells, exogenous methionine provided protection from GSNO-mediated killing but not from NO-mediated killing. Anaerobic exposure to NO led to up-regulation of multiple Fnr-repressed genes and down-regulation of Fnr-activated genes, including nrfA, which encodes cytochrome c nitrite reductase, providing strong evidence that there is NO inactivation of Fnr. Other global regulators apparently affected by NO were IscR, Fur, SoxR, NsrR, and NorR. We tried to identify components of the NorR regulon by performing a microarray comparison of NO-exposed wild-type and norR mutant strains; only norVW, encoding the NO-detoxifying flavorubredoxin and its cognate reductase, were unambiguously identified. Mutation of norV or norR had no effect on E. coli survival in mouse macrophages. Thus, GSNO (a nitrosating agent) and NO have distinct cellular effects; NO more effectively interacts with global regulators that mediate adaptive responses to nitrosative stress but does not affect methionine requirements arising from homocysteine nitrosation.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=17189370 PubMed]
Online version:[http://dx.doi.org/10.1128/JB.01354-06 10.1128/JB.01354-06]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{| id="Y4dfa76180bf7b" class=" tableEdit GO_table_reference dataTable"
|- {{table heading style}}
!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=63ce1649aab8b3180235b0af7618f667.177918.Y4dfa76180bf7b&page=177918&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE5075 GEO Page: E-GEOD-5075]
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE5076 GEO Page: E-GEOD-5076]
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE5137 GEO Page: E-GEOD-5137]
# [http://www.ncbi.nlm.nih.gov/projects/geo/query/acc.cgi?acc=GSE5139 GEO Page: E-GEOD-5139]
# [http://smd.stanford.edu/cgi-bin/publication/viewPublication.pl?pub_no=1034 SMD Publication]
# [http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-GEOD-5098&species=&array=&exptype%5B%5D=&exptype%5B%5D=&pagesize=25&sortby=releasedate&sortorder=descending&expandefo=on ArrayExpress Accession: E-GEOD-5098]

==References==
{{RefHelp}}
<references/>

PMID:21057108

2011-06-28T18:44:38Z

Mdmueller: /* See also */

{{RightTOC}}
<protect>
 '''Conrad, TM, Frazier, M, Joyce, AR, Cho, BK, Knight, EM, Lewis, NE, Landick, R and Palsson, BØ''' (2010) RNA polymerase mutants found through adaptive evolution reprogram Escherichia coli for optimal growth in minimal media.''Proc. Natl. Acad. Sci. U.S.A.'' '''107''':20500-5

{|{{Prettytable}} align = 'center' width= '70%'
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|{{TableHeadingColor}} |'''Abstract''' || <protect>Specific small deletions within the rpoC gene encoding the β'-subunit of RNA polymerase (RNAP) are found repeatedly after adaptation of Escherichia coli K-12 MG1655 to growth in minimal media. Here we present a multiscale analysis of these mutations. At the physiological level, the mutants grow 60% faster than the parent strain and convert the carbon source 15-35% more efficiently to biomass, but grow about 30% slower than the parent strain in rich medium. At the molecular level, the kinetic parameters of the mutated RNAP were found to be altered, resulting in a 4- to 30-fold decrease in open complex longevity at an rRNA promoter and a ∼10-fold decrease in transcriptional pausing, with consequent increase in transcript elongation rate. At a genome-scale, systems biology level, gene expression changes between the parent strain and adapted RNAP mutants reveal large-scale systematic transcriptional changes that influence specific cellular processes, including strong down-regulation of motility, acid resistance, fimbria, and curlin genes. RNAP genome-binding maps reveal redistribution of RNAP that may facilitate relief of a metabolic bottleneck to growth. These findings suggest that reprogramming the kinetic parameters of RNAP through specific mutations allows regulatory adaptation for optimal growth in new environments.</protect>
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|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=21057108 PubMed]
Online version:[http://dx.doi.org/10.1073/pnas.0911253107 10.1073/pnas.0911253107]
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==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
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{| id="K4e036ef80be42" class=" tableEdit GO_table_reference dataTable"
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!|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

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</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==See also==
# [http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE15500 GEO Page: E-GEOD-15500]
# [http://www.ebi.ac.uk/arrayexpress/browse.html?keywords=E-GEOD-15500&expandefo=on ArrayExpress Accession: E-GEOD-15500]

==References==
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<references/>