EcoliWiki - User contributions [en]

PMID:1917875

2014-04-28T18:07:54Z

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'''Schmitt, CK, Kemp, P and Molineux, IJ''' (1991) Genes 1.2 and 10 of bacteriophages T3 and T7 determine the permeability lesions observed in infected cells of Escherichia coli expressing the F plasmid gene pifA. ''J. Bacteriol.'' '''173''':6507-14
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!align=left |Abstract
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Infections of F plasmid-containing strains of Escherichia coli by bacteriophage T7 result in membrane damage that allows nucleotides to exude from the infected cell into the culture medium. Only pifA of the F pif operon is necessary for "leakiness" of the T7-infected cell. Expression of either T7 gene 1.2 or gene 10 is sufficient to cause leakiness, since infections by phage containing null mutations in both of these genes do not result in permeability changes of the F-containing cell. Even in the absence of phage infection, expression from plasmids of either gene 1.2 or 10 can cause permeability changes, particularly of F plasmid-containing cells. In contrast, gene 1.2 of the related bacteriophage T3 prevents leakiness of the infected cell. In the absence of T3 gene 1.2 function, expression of gene 10 causes membrane damage that allows nucleotides to leak from the cell. Genes 1.2 and 10 of both T3 and T7 are the two genes involved in determining resistance or sensitivity to F exclusion; F exclusion and leakiness of the phage-infected cell are therefore closely related phenomena. However, since leakiness of the infected cell does not necessarily result in phage exclusion, it cannot be used as a predictor of an abortive infection.
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=1917875 PubMed] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC208987 PMC208987]

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Cell Membrane Permeability/genetics; Escherichia coli/genetics; Escherichia coli/metabolism; F Factor/genetics; Gene Expression/physiology; Genes, Viral/genetics; Nucleotides/analysis; Operon/genetics; T-Phages/genetics

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PMID:1917875

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PMID:6233425

2014-04-09T17:36:52Z

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'''Miki, T, Chang, ZT and Horiuchi, T''' (1984) Control of cell division by sex factor F in Escherichia coli. II. Identification of genes for inhibitor protein and trigger protein on the 42.84-43.6 F segment. ''J. Mol. Biol.'' '''174''':627-46
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The genetic structure of the 42.84-43.6 F (BamHI-PstI) segment of the F plasmid, which contains all the F DNA sequences necessary for coupling cell division of F+ bacteria with plasmid DNA replication, was analyzed by isolating a series of amber mutants. Two cistrons were found in this region and they were designated letA and letD (an abbreviation for lethal mutation). The letA and letD cistrons were mapped on the 42.84-43.35 F (BamHI- XmaI ) segment and the 43.07-43.6 F (HincII-PstI) segment, respectively, and are presumed to correspond to the first (43.04-43.26 F) and second (43.26-43.57 F) open reading frames, respectively, which were found in this region by nucleotide sequencing. The letD gene product acts to inhibit cell division of the host bacteria and to induce prophages in lysogenic bacteria, whereas the letA gene product acts to suppress the activity of the letD gene product. Taking into consideration the fact that the 42.84-43.6 F segment carries all the F plasmid genes necessary for coupling cell division with plasmid DNA replication, and that the expression of the genes is likely to be controlled by plasmid DNA replication, we constructed the following hypothesis. Before completion of plasmid DNA replication, LetD protein acts to prevent cell division of the host bacteria. When plasmid DNA replication is completed, synthesis of LetA protein (and also LetD protein) takes place and the LetA protein synthesized acts to suppress the activity of LetD protein and make the cell ready for cell division. Actual cell division will take place when replication of both chromosomal and plasmid DNA is completed and the termination protein of the chromosome and the LetA protein of F plasmid are both synthesized. When cell division takes place LetA protein is consumed, and as a result LetD protein becomes active and prevents cell division until the next round of DNA replication is completed.
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=6233425 PubMed]

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!align=left |Keywords
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Bacteriophage lambda; Cell Division; Escherichia coli/cytology; Escherichia coli/drug effects; Escherichia coli/genetics; F Factor; Gene Expression Regulation; Genes; Genes, Bacterial; Genes, Lethal; Mutation; Nalidixic Acid/pharmacology; Suppression, Genetic; Virus Activation

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PMID:6233425

2014-04-09T17:36:51Z

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PMID:2830275

2014-03-17T17:53:12Z

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'''Lahue, EE and Matson, SW''' (1988) Escherichia coli DNA helicase I catalyzes a unidirectional and highly processive unwinding reaction. ''J. Biol. Chem.'' '''263''':3208-15
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Helicase I has been purified to greater than 95% homogeneity from an F+ strain of Escherichia coli, and characterized as a single-stranded DNA-dependent ATPase and a helicase. The duplex DNA unwinding reaction requires a region of ssDNA for enzyme binding and concomitant nucleoside 5'-triphosphate hydrolysis. All eight predominant nucleoside 5'-triphosphates can satisfy this requirement. Unwinding is unidirectional in the 5' to 3' direction. The length of duplex DNA unwound is independent of protein concentration suggesting that the unwinding reaction is highly processive. Kinetic analysis of the unwinding reaction indicates that the enzyme turns over very slowly from one DNA substrate molecule to another. The ATP hydrolysis reaction is continuous when circular partial duplex DNA substrates are used as DNA effectors. When linear partial duplex substrates are used ATP hydrolysis is barely detectable, although the kinetics of the unwinding reaction on linear partial duplex substrates are identical to those observed using a circular partial duplex DNA substrate. This suggests that ATP hydrolysis fuels continuous translocation of helicase I on circular single-stranded DNA while on linear single stranded DNA the enzyme translocates to the end of the DNA molecule where it must slowly dissociate from the substrate molecule and/or slowly associate with a new substrate molecule, thus resulting in a very low rate of ATP hydrolysis.
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=2830275 PubMed]

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Adenosine Triphosphatases/metabolism; Adenosine Triphosphate/metabolism; DNA/metabolism; DNA Helicases/isolation & purification; DNA Helicases/metabolism; DNA, Circular/metabolism; DNA, Single-Stranded/metabolism; Escherichia coli/enzymology; Escherichia coli Proteins; Hydrolysis; Kinetics; Substrate Specificity

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PMID:2830275

2014-03-17T17:53:11Z

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PMID:4607804

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'''Lengyel, JA, Goldstein, RN, Marsh, M and Calendar, R''' (1974) Structure of the bacteriophage P2 tail. ''Virology'' '''62''':161-74
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No abstract in PubMed
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=4607804 PubMed]

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!align=left |Keywords
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Autoradiography; Carbon Radioisotopes; Chromosome Mapping; Coliphages/analysis; Coliphages/metabolism; Coliphages/ultrastructure; DNA Viruses; Electrophoresis, Polyacrylamide Gel; Escherichia coli; Genes; Microscopy, Electron; Molecular Weight; Mutation; Sulfur Radioisotopes; Temperature; Viral Proteins/analysis; Viral Proteins/biosynthesis

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PMID:4607804

2014-02-11T21:00:07Z

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PMID:23090957

2013-03-29T21:51:00Z

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'''Withman, B , Gunasekera, TS , Beesetty, P , Agans, R and Paliy, O ''' (2013) Transcriptional responses of uropathogenic Escherichia coli to increased environmental osmolality caused by salt or urea. ''Infect. Immun.'' '''81''':80-9
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Uropathogenic Escherichia coli (UPEC) is the most common causative agent of urinary tract infections in humans. The majority of urinary infections develop via ascending route through the urethra, where bacterial cells come in contact with human urine prior to reaching the bladder or kidneys. Since urine contains significant amounts of inorganic ions and urea, it imposes osmotic and denaturing stresses on bacterial cells. In this study, we determined the transcriptional adaptive responses of UPEC strain CFT073 to the presence of 0.3 M NaCl or 0.6 M urea in the growth medium. The cell responses to these two osmolytes were drastically different. Although most of the genes of the osmotically inducible regulon were overexpressed in medium with salt, urea failed to stimulate osmotic stress response. At the same time, UPEC colonization genes encoding type 1 and F1C fimbriae and capsule biosynthesis were transcriptionally induced in the presence of urea but did not respond to increased salt concentration. We speculate that urea can potentially be sensed by uropathogenic bacteria to initiate infection program. In addition, several molecular chaperone genes were overexpressed in the presence of urea, whereas adding NaCl to the medium led to an upregulation of a number of anaerobic metabolism pathways.
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=23090957 PubMed] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3536127 PMC3536127]
Online version:[http://dx.doi.org/10.1128/IAI.01049-12 10.1128/IAI.01049-12]
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{| border="2" cellpadding="4" cellspacing="0" style="margin: 1em 1em 1em 0; border: 1px #aaa solid; border-collapse: collapse;" id="J51560cc426aa8" 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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PMID:23090957

2013-03-29T21:50:59Z

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PMID:22684885

2013-03-25T21:09:26Z

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'''Wang, J , Zhang, Y , Chen, Y , Lin, M and Lin, Z ''' (2012) Global regulator engineering significantly improved Escherichia coli tolerances toward inhibitors of lignocellulosic hydrolysates. ''Biotechnol. Bioeng.'' '''109''':3133-42
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Lignocellulosic biomass is regarded as the most viable source of feedstock for industrial biorefinery, but the harmful inhibitors generated from the indispensable pretreatments prior to fermentation remain a daunting technical hurdle. Using an exogenous regulator, irrE, from the radiation-resistant Deinococcus radiodurans, we previously showed that a novel global regulator engineering (GRE) approach significantly enhanced tolerances of Escherichia coli to alcohol and acetate stresses. In this work, an irrE library was subjected to selection under various stresses of furfural, a typical hydrolysate inhibitor. Three furfural tolerant irrE mutants including F1-37 and F2-1 were successfully obtained. The cells containing these mutants reached OD(600) levels of 4- to 16-fold of that for the pMD18T cells in growth assay under 0.2% (v/v) furfural stress. The cells containing irrE F1-37 and F2-1 also showed considerably reduced intracellular oxygen species (ROS) levels under furfural stress. Moreover, these two irrE mutants were subsequently found to confer significant cross tolerances to two other most common inhibitors, 5-hydroxymethyl-2-furaldehyde (HMF), vanillin, as well as real lignocellulosic hydrolysates. When evaluated in Luria-Bertani (LB) medium supplemented with corn stover cellulosic hydrolysate (prepared with a solid loading of 30%), the cells containing the mutants exhibited lag phases markedly shortened by 24-44 h in comparison with the control cells. This work thus presents a promising step forward to resolve the inhibitor problem for E. coli. From the view of synthetic biology, irrE can be considered as an evolvable "part" for various stresses. Furthermore, this GRE approach can be extended to exploit other exogenous global regulators from extremophiles, and the native counterparts in E. coli, for eliciting industrially useful phenotypes.
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=22684885 PubMed]
Online version:[http://dx.doi.org/10.1002/bit.24574 10.1002/bit.24574]
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Biomass; Bioreactors/microbiology; Escherichia coli/genetics; Escherichia coli/metabolism; Escherichia coli/physiology; Furaldehyde/chemistry; Furaldehyde/metabolism; Genetic Engineering/methods; Lignin/antagonists & inhibitors; Lignin/metabolism; Models, Molecular; Mutation; Polysaccharides/metabolism; Reactive Oxygen Species/metabolism; Sequence Alignment

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==Significance {{HelpIcon|Help:Literature}} ==
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{| border="2" cellpadding="4" cellspacing="0" style="margin: 1em 1em 1em 0; border: 1px #aaa solid; border-collapse: collapse;" id="C5150bd0681f76" 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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PMID:22684885

2013-03-25T21:09:26Z

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PMID:2022622

2012-06-29T00:01:54Z

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'''Shah, S and Peterkofsky, A''' (1991) Characterization and generation of Escherichia coli adenylate cyclase deletion mutants.''J. Bacteriol.'' '''173''':3238-42
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Escherichia coli delta cya-283 is a 75-bp in-frame deletion overlapping the 5' end of delta cya-854; delta cya-201 is a 41-bp frameshift deletion overlapping the 3' end of delta cya-854. Sequence repeats were found at the boundaries of delta cya-283 and delta cya-201, suggesting a mechanism for deletion formation. Recombinant DNA procedures were used to construct a strain in which the total cya structural gene in the chromosome was replaced by the kanamycin resistance gene.
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=2022622 PubMed]

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Adenylate Cyclase; Base Sequence; Chromosome Deletion; DNA Mutational Analysis; DNA, Bacterial; Escherichia coli; Genes, Bacterial; Genetic Vectors; Molecular Sequence Data; Polymerase Chain Reaction; Restriction Mapping

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{| id="G4fecf07214ff6" 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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PMID:2022622

2012-06-29T00:01:53Z

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PMID:201606

2012-06-29T00:01:20Z

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'''Alper, MD and Ames, BN''' (1978) Transport of antibiotics and metabolite analogs by systems under cyclic AMP control: positive selection of Salmonella typhimurium cya and crp mutants.''J. Bacteriol.'' '''133''':149-57
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!align=left |Abstract
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Mutants in the cyclic AMP (cAMP) control system in Salmonella typhimurium (cya = adenyl cyclase, crp = cAMP receptor protein) were partially resistant to growth inhibition by 22 antibiotics (including fosfomycin, nalidixic acid, and streptomycin) and 29 inhibitory analogs of normal bacterial fuel/carbon sources. This resistance was used as the basis for an efficient positive selection of cya and crp mutants. We propose that these antibiotics and analogs enter the bacteria through transport systems normally used for transporting fuel/carbon sources and that this is accomplished because of a structural similarity between the antibiotic and the natural substrate of the particular transport system involved. We propose that these transport systems are all under positive control by cAMP and that cAMP acts as a signal molecule (alarmone) for fuel/carbon deprivation. Evidence is provided for a hierarchy within operons controlled by cAMP. The methodology is shown to be useful for analyzing both antibiotic transport systems and the cAMP super-control system.
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=201606 PubMed]

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Amino Acids; Anti-Bacterial Agents; Biological Transport; Cyclic AMP; Drug Resistance, Microbial; Mutation; Salmonella typhimurium

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{| id="J4fecf0503d8ca" 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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PMID:201606

2012-06-29T00:01:19Z

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PMID:168178

2012-06-28T23:59:15Z

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'''Alper, MD and Ames, BN''' (1975) Cyclic 3', 5'-adenosine monophosphate phosphodiesterase mutants of Salmonella typhimurium.''J. Bacteriol.'' '''122''':1081-90
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Positive selection procedures for mutants of Salmonella typhimurium lacking cyclic 3', 5'7-adenosine monophosphate (cAMP) phosphodiesterase have been devised. The gene (cpd) coding for this enzyme has been located on the chromosome and shown to be 25% co-transducible with metC using phage P22. The mutants have been used to investigate the role of the enzyme in the control of genes whose expression is known to be dependent on cAMP. Significant alterations in the regulation of some but not others of these genes have been observed in these mutants. Mutants lacking the cAMP phosphodiesterase are more sensitive than their parents to a variety of antibiotics that appear to enter the cell through cAMP-dependent transport systems. They grow faster than the wild type on succinate-ammonia-salts, and glucose-proline-salts media and are inhibited by added cAMP on glucose, citrate, or glycerol-ammonia salts media whereas the wild type is unaffected. Neither the growth of Salmonella typhimurium on glycerol or citrate media nor the level of acid hexose phosphatase in the strain is affected by the loss of cAMP phosphodiesterase. In addition, the mutant strains are extremely sensitive to high levels of cAMP. Loss of the cAMP phosphodiesterase in strains unable to synthesize cAMP (adenyl cyclase negative) reduces by 10-fold the requirement for exogenous cAMP for expression of catabolite-sensitive phenotypes. These results suggest that through its control of cAMP levels in the cell the phosphodiesterase may be involved in the regulation of certain classes of catabolite-sensitive operaons and also in protecting the cell against high levels of cAMP.
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=168178 PubMed]

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!align=left |Keywords
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3',5'-Cyclic-AMP Phosphodiesterases; Acid Phosphatase; Adenylate Cyclase; Ammonia; Anti-Bacterial Agents; Cell-Free System; Chromosome Mapping; Citrates; Cyclic AMP; Drug Resistance, Microbial; Genes; Glucose; Glycerol; Mutation; Phosphoric Diester Hydrolases; Proline; Salmonella typhimurium; Succinates; Temperature; Transduction, Genetic

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{| id="Q4fecefd2e6b34" 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"
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|}
</protect>

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

==See also==

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

PMID:168178

2012-06-28T23:59:14Z

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PMID:2477224

2012-05-14T21:52:57Z

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{| id="I4fb17ea62c0e2" class=" tableEdit PMID_info_table"

|-
!align=left |Citation
||
'''Bar, RS, Booth, BA, Boes, M and Dake, BL''' (1989) Insulin-like growth factor-binding proteins from vascular endothelial cells: purification, characterization, and intrinsic biological activities.''Endocrinology'' '''125''':1910-20
|-
!align=left |Abstract
||
Insulin-like growth factor (IGF)-binding proteins are produced by several cell types, including vascular endothelial cells. The production of IGF-binding proteins by endothelial cells is of particular interest, since these cells are directly bathed by the circulating IGFs and form the initial barrier to the passage of circulating IGFs from the bloodstream to subendothelial tissues. We have purified IGF-binding proteins from medium conditioned by cultured bovine endothelial cells by sequential passage over Bio-Gel P-60, multiplication-stimulating activity affinity, anion exchange (DEAE cellulose) and/or hydrophobic (phenyl-Sepharose) chromatography. Two peaks of IGF-binding activity were eluted from the phenyl-Sepharose column. After cross-linking, each peak contained two to five protein bands on gels that specifically bound IGF-I and -II with mol wt ranging from about 28-44K. Material in peak 1 bound IGF-I congruent to IGF-II and had no affinity for insulin and proinsulin. Peak 2 IGF-binding proteins bound IGF-II with substantially higher affinity than IGF-I and did not recognize insulin or proinsulin. Peak 1 material from phenyl-Sepharose chromatography was a potent stimulator of both glucose transport and aminoisobutyric acid (AIB) uptake in microvessel endothelial cells, with maximal stimulation of both processes being 300-400% of control values. In contrast, peak 2 material either had no intrinsic bioactivity or was slightly inhibitory or stimulatory, depending on the concentration of peak 2 material that was added. The bioactivity in peak 1 was not due to copurification of other endothelial proteins capable of stimulating glucose and AIB uptake, such as IGF-I/-II, platelet-derived growth factor, and basic fibroblast growth factor, since bioactivity was retained after acid treatment, antibody neutralization, and selective affinity chromatography to deplete these other factors. When peak 1 material was added to IGF-I the bioeffects (glucose and AIB uptake) of IGF and binding proteins were additive, and in some experiments the binding proteins potentiated the effect of IGF on endothelial cells, suggesting that the binding protein-IGF complex may retain the bioactivity of both the binding protein(s) and the IGF.
|-
!align=left |Links
||
[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=2477224 PubMed]

|-
!align=left |Keywords
||
Animals; Binding, Competitive; Biomechanics; Carrier Proteins; Cells, Cultured; Endothelium, Vascular; Insulin; Insulin-Like Growth Factor Binding Proteins; Proinsulin; Somatomedins

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=d41d8cd98f00b204e9800998ecf8427e.182385.I4fb17ea62c0e2&page=182385&pagename={{FULLPAGENAMEE}}&type=1&template=PMID_info_table edit table] ||
|}


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

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{{LitMaterials}}

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

{| id="P4fb17eb88dee1" 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=d41d8cd98f00b204e9800998ecf8427e.182385.P4fb17eb88dee1&page=182385&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
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==References==
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<references/>

PMID:2477224

2012-05-14T21:52:30Z

165.91.108.111: New PMID: Page!

PMID:22342931

2012-05-09T17:07:28Z

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{| id="Z4faaa44fd9170" class=" tableEdit PMID_info_table"

|-
!align=left |Citation
||
'''Tomko, EJ, Fischer, CJ and Lohman, TM''' (2012) Single-stranded DNA translocation of E. coli UvrD monomer is tightly coupled to ATP hydrolysis.''J. Mol. Biol.'' '''418''':32-46
|-
!align=left |Abstract
||
Escherichia coli UvrD is an SF1A (superfamily 1 type A) helicase/translocase that functions in several DNA repair pathways. A UvrD monomer is a rapid and processive single-stranded DNA (ssDNA) translocase but is unable to unwind DNA processively in vitro. Based on data at saturating ATP (500 μM), we proposed a nonuniform stepping mechanism in which a UvrD monomer translocates with biased (3' to 5') directionality while hydrolyzing 1 ATP per DNA base translocated, but with a kinetic step size of 4-5 nt/step, suggesting that a pause occurs every 4-5 nt translocated. To further test this mechanism, we examined UvrD translocation over a range of lower ATP concentrations (10-500 μM ATP), using transient kinetic approaches. We find a constant ATP coupling stoichiometry of ∼1 ATP/DNA base translocated even at the lowest ATP concentration examined (10 μM), indicating that ATP hydrolysis is tightly coupled to forward translocation of a UvrD monomer along ssDNA with little slippage or futile ATP hydrolysis during translocation. The translocation kinetic step size remains constant at 4-5 nt/step down to 50 μM ATP but increases to ∼7 nt/step at 10 μM ATP. These results suggest that UvrD pauses more frequently during translocation at low ATP but with little futile ATP hydrolysis.
|-
!align=left |Links
||
[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=22342931 PubMed]
Online version:[http://dx.doi.org/10.1016/j.jmb.2012.02.013 10.1016/j.jmb.2012.02.013]
|-
!align=left |Keywords
||

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=d41d8cd98f00b204e9800998ecf8427e.181982.Z4faaa44fd9170&page=181982&pagename={{FULLPAGENAMEE}}&type=1&template=PMID_info_table edit table] ||
|}


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

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{{LitMaterials}}

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<protect>

{| id="B4faaa45023c07" 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=d41d8cd98f00b204e9800998ecf8427e.181982.B4faaa45023c07&page=181982&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

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

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

PMID:22342931

2012-05-09T17:07:27Z

165.91.108.111: New PMID: Page!

PMID:6229530

2012-05-03T17:57:45Z

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{| id="G4fa2c717dba5f" class=" tableEdit PMID_info_table"

|-
!align=left |Citation
||
'''Friedman, DI, Olson, EJ, Carver, D and Gellert, M''' (1984) Synergistic effect of himA and gyrB mutations: evidence that him functions control expression of ilv and xyl genes.''J. Bacteriol.'' '''157''':484-9
|-
!align=left |Abstract
||
We have constructed Escherichia coli strains containing mutations at two different loci, both originally selected for failure to support lambda site-specific recombination: himA and gyrB-him(Ts). Although the gyrB-him(Ts) mutations by themselves reduce supercoiling at high temperature, the double mutants show a far greater effect on supercoiling. Our studies show that growth of phage lambda is severely inhibited and that maintenance of plasmid pBR322 is extremely unstable in the double mutants. Physiological studies also reveal that the double mutants are isoleucine auxotrophs at 42 degrees C. The fact that himA mutants are isoleucine auxotrophs at 42 degrees C in the presence of leucine suggests that a significant component of the isoleucine auxotrophy of the double mutants is a result of the himA mutation. The himA gene encodes the alpha subunit of a protein called the integration host factor. Since mutations in the hip or himD gene encoding beta, the other subunit of the integration host factor, also result in isoleucine auxotrophy in the presence of leucine, we suggest that the integration host factor regulates the synthesis of at least one of the enzymes in the ilv pathway, acetohydroxyacid synthase I, which is encoded by the ilvB gene. Studies of the utilization of various sugars as the sole carbon source suggest that the integration host factor controls expression of some gene(s) involved in the utilization of xylose.
|-
!align=left |Links
||
[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=6229530 PubMed]

|-
!align=left |Keywords
||
Bacteriophage lambda; DNA, Superhelical; Escherichia coli; Genes, Bacterial; Genes, Viral; Monosaccharides; Mutation; Viral Proteins

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=d41d8cd98f00b204e9800998ecf8427e.181788.G4fa2c717dba5f&page=181788&pagename={{FULLPAGENAMEE}}&type=1&template=PMID_info_table edit table] ||
|}


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

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{{LitMaterials}}

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<protect>

{| id="S4fa2c718d9a07" 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=d41d8cd98f00b204e9800998ecf8427e.181788.S4fa2c718d9a07&page=181788&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
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==References==
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<references/>

PMID:6229530

2012-05-03T17:57:43Z

165.91.108.111: New PMID: Page!

PMID:21143325

2012-04-20T22:41:17Z

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{| id="O4f91e60c79d43" class=" tableEdit PMID_info_table"

|-
!align=left |Citation
||
'''Ozyamak, E, Black, SS, Walker, CA, Maclean, MJ, Bartlett, W, Miller, S and Booth, IR''' (2010) The critical role of S-lactoylglutathione formation during methylglyoxal detoxification in Escherichia coli.''Mol. Microbiol.'' '''78''':1577-90
|-
!align=left |Abstract
||
Survival of exposure to methylglyoxal (MG) in Gram-negative pathogens is largely dependent upon the operation of the glutathione-dependent glyoxalase system, consisting of two enzymes, GlxI (gloA) and GlxII (gloB). In addition, the activation of the KefGB potassium efflux system is maintained closed by glutathione (GSH) and is activated by S-lactoylGSH (SLG), the intermediate formed by GlxI and destroyed by GlxII. Escherichia coli mutants lacking GlxI are known to be extremely sensitive to MG. In this study we demonstrate that a ΔgloB mutant is as tolerant of MG as the parent, despite having the same degree of inhibition of MG detoxification as a ΔgloA strain. Increased expression of GlxII from a multicopy plasmid sensitizes E. coli to MG. Measurement of SLG pools, KefGB activity and cytoplasmic pH shows these parameters to be linked and to be very sensitive to changes in the activity of GlxI and GlxII. The SLG pool determines the activity of KefGB and the degree of acidification of the cytoplasm, which is a major determinant of the sensitivity to electrophiles. The data are discussed in terms of how cell fate is determined by the relative abundance of the enzymes and KefGB.
|-
!align=left |Links
||
[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=21143325 PubMed]
Online version:[http://dx.doi.org/10.1111/j.1365-2958.2010.07426.x 10.1111/j.1365-2958.2010.07426.x]
|-
!align=left |Keywords
||
Escherichia coli; Escherichia coli Proteins; Glutathione; Lactoylglutathione Lyase; Microbial Viability; Potassium-Hydrogen Antiporters; Pyruvaldehyde

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=d41d8cd98f00b204e9800998ecf8427e.181654.O4f91e60c79d43&page=181654&pagename={{FULLPAGENAMEE}}&type=1&template=PMID_info_table edit table] ||
|}


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

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{{LitMaterials}}

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<protect>

{| id="F4f91e60d08600" 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=d41d8cd98f00b204e9800998ecf8427e.181654.F4f91e60d08600&page=181654&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
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{{RefHelp}}
<references/>

PMID:21143325

2012-04-20T22:41:16Z

165.91.108.111: New PMID: Page!

PMID:21889449

2012-04-17T22:49:49Z

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{| id="H4f8df38ca7d1a" class=" tableEdit PMID_info_table"

|-
!align=left |Citation
||
'''Chakrabarti, J, Chandra, N, Raha, P and Roy, S''' (2011) High-affinity quasi-specific sites in the genome: how the DNA-binding proteins cope with them.''Biophys. J.'' '''101''':1123-9
|-
!align=left |Abstract
||
Many prokaryotic transcription factors home in on one or a few target sites in the presence of a huge number of nonspecific sites. Our analysis of λ-repressor in the Escherichia coli genome based on single basepair substitution experiments shows the presence of hundreds of sites having binding energy within 3 Kcal/mole of the O(R)1 binding energy, and thousands of sites with binding energy above the nonspecific binding energy. The effect of such sites on DNA-based processes has not been fully explored. The presence of such sites dramatically lowers the occupation probability of the specific site far more than if the genome were composed of nonspecific sites only. Our Brownian dynamics studies show that the presence of quasi-specific sites results in very significant kinetic effects as well. In contrast to λ-repressor, the E. coli genome has orders of magnitude lower quasi-specific sites for GalR, an integral transcription factor, thus causing little competition for the specific site. We propose that GalR and perhaps repressors of the same family have evolved binding modes that lead to much smaller numbers of quasi-specific sites to remove the untoward effects of genomic DNA.
|-
!align=left |Links
||
[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=21889449 PubMed]
Online version:[http://dx.doi.org/10.1016/j.bpj.2011.07.041 10.1016/j.bpj.2011.07.041]
|-
!align=left |Keywords
||
Binding Sites; DNA-Binding Proteins; Escherichia coli; Escherichia coli Proteins; Genome, Bacterial; Kinetics; Models, Biological; Repressor Proteins; Thermodynamics; Viral Regulatory and Accessory Proteins

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=d41d8cd98f00b204e9800998ecf8427e.181450.H4f8df38ca7d1a&page=181450&pagename={{FULLPAGENAMEE}}&type=1&template=PMID_info_table edit table] ||
|}


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

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{{LitMaterials}}

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

{| id="K4f8df38d0503b" 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=d41d8cd98f00b204e9800998ecf8427e.181450.K4f8df38d0503b&page=181450&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
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{{RefHelp}}
<references/>

PMID:21889449

2012-04-17T22:49:48Z

165.91.108.111: New PMID: Page!

PMID:2112211

2012-04-14T00:42:50Z

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{| id="X4f88c80aac9a4" class=" tableEdit PMID_info_table"

|-
!align=left |Citation
||
'''Ichikawa, S, Wakao, Y, Muto, M and Takahashi, M''' (1990) Experimental studies of the load reducing effects of nitroglycerin in heart failure.''Nippon Juigaku Zasshi'' '''52''':361-9
|-
!align=left |Abstract
||
The load-reducing effect of nitroglycerin (NTG), a vasodilator, was studied in dogs with heart failure. The chordae tendineae of the mitral valve were transected to induce acute mitral regurgitation (MR) for hemodynamic evaluation. By such surgical treatment, preload indices such as left ventricular end-diastolic pressure (LVEDP) and left atrial pressure (LAP) increased significantly, and subsequent cardiac dysfunction and heart failure were indicated by another decrease in stroke volume, myocardial contractility, forward flow, and myocardial oxygen consumption. To dogs with artificially established acute MR, 3 micrograms/kg/min of NTG was administered intra-arterially by means of a continuous infusion, that resulted in decrease of LVEDP, LAP and central venous pressure (CVP). Thus, a reduction of preload was determined. Simultaneously, afterload indices such as aortic systolic pressure (Aos), aortic mean pressure (Aom) and total peripheral resistance (TPR) decreased remarkably. Afterload reduction depended on the amount of venous return; therefore, an extra-corporeal circulation system was applied in order to supply a constant venous return before NTG administration. This caused a significant decrease in aortic diastolic pressure (Aod), Aos, Aom, left ventricular systolic pressure (LVSP) and TPR, and an increase in myocardial contractility and cardiac output. This suggested that afterload reduction might be realized by the vasodilatory effect of NTG on the resistance vessels.
|-
!align=left |Links
||
[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=2112211 PubMed]

|-
!align=left |Keywords
||
Animals; Blood Pressure; Chordae Tendineae; Dogs; Female; Heart Failure; Male; Mitral Valve Insufficiency; Myocardial Contraction; Nitroglycerin; Oxygen Consumption; Stroke Volume

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=d41d8cd98f00b204e9800998ecf8427e.181262.X4f88c80aac9a4&page=181262&pagename={{FULLPAGENAMEE}}&type=1&template=PMID_info_table edit table] ||
|}


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

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{{LitMaterials}}

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<protect>

{| id="I4f88c80abadca" 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=d41d8cd98f00b204e9800998ecf8427e.181262.I4f88c80abadca&page=181262&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

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{{RefHelp}}
<references/>

PMID:2112211

2012-04-14T00:42:50Z

165.91.108.111: New PMID: Page!

PMID:22422986

2012-04-11T22:09:46Z

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{| id="I4f860129035c7" class=" tableEdit PMID_info_table"

|-
!align=left |Citation
||
'''Gagnon, MG, Seetharaman, SV, Bulkley, D and Steitz, TA''' (2012) Structural basis for the rescue of stalled ribosomes: structure of YaeJ bound to the ribosome.''Science'' '''335''':1370-2
|-
!align=left |Abstract
||
In bacteria, the hybrid transfer-messenger RNA (tmRNA) rescues ribosomes stalled on defective messenger RNAs (mRNAs). However, certain gram-negative bacteria have evolved proteins that are capable of rescuing stalled ribosomes in a tmRNA-independent manner. Here, we report a 3.2 angstrom-resolution crystal structure of the rescue factor YaeJ bound to the Thermus thermophilus 70S ribosome in complex with the initiator tRNA(i)(fMet) and a short mRNA. The structure reveals that the C-terminal tail of YaeJ functions as a sensor to discriminate between stalled and actively translating ribosomes by binding in the mRNA entry channel downstream of the A site between the head and shoulder of the 30S subunit. This allows the N-terminal globular domain to sample different conformations, so that its conserved GGQ motif is optimally positioned to catalyze the hydrolysis of peptidyl-tRNA. This structure gives insights into the mechanism of YaeJ function and provides a basis for understanding how it rescues stalled ribosomes.
|-
!align=left |Links
||
[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=22422986 PubMed]
Online version:[http://dx.doi.org/10.1126/science.1217443 10.1126/science.1217443]
|-
!align=left |Keywords
||
Amino Acid Sequence; Carboxylic Ester Hydrolases; Crystallography, X-Ray; Escherichia coli; Escherichia coli Proteins; Models, Molecular; Molecular Sequence Data; Nucleic Acid Conformation; Protein Biosynthesis; Protein Structure, Tertiary; RNA, Bacterial; RNA, Messenger; RNA, Ribosomal; RNA, Transfer, Amino Acyl; RNA, Transfer, Met; Ribosome Subunits, Large, Bacterial; Ribosome Subunits, Small, Bacterial; Ribosomes; Thermus thermophilus

|- class="tableEdit_footer"
|[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=d41d8cd98f00b204e9800998ecf8427e.181018.I4f860129035c7&page=181018&pagename={{FULLPAGENAMEE}}&type=1&template=PMID_info_table edit table] ||
|}


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

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{{LitMaterials}}

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<protect>

{| id="U4f86012a86513" 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=d41d8cd98f00b204e9800998ecf8427e.181018.U4f86012a86513&page=181018&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
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{{RefHelp}}
<references/>

PMID:22422986

2012-04-11T22:09:44Z

165.91.108.111: New PMID: Page!

PMID:8466900

2011-10-18T15:22:43Z

165.91.108.111: Fill PMID: Page!

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<protect>
 '''Zwiefka, A, Kohn, H and Widger, WR''' (1993) Transcription termination factor rho: the site of bicyclomycin inhibition in Escherichia coli.''Biochemistry'' '''32''':3564-70

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>Bicyclomycin is a novel, commercially important antibiotic. Information concerning the site of bicyclomycin inhibition in Escherichia coli has been obtained by the production of bicyclomycin resistant mutants by UV irradiation. Selection by growth in the presence of bicyclomycin of a plasmid clone library generated from a highly resistant mutant in recipient antibiotic-sensitive host cells (E. coli strain W3350) has led to the characterization of three different plasmids that confer drug resistance, which contained the gene encoding the transcription termination factor, rho. These mutant rho genes contained single base changes at nucleotide positions 656, 796, and 1009. Preliminary mechanistic information has been obtained by monitoring the polyC-dependent ATPase activity of rho in the absence and presence of bicyclomycin and dihydrobicyclomycin. Addition of bicyclomycin to aqueous solutions containing rho and ATP led to a decrease in the release of inorganic phosphate with an I50 value of 60-70 microM bicyclomycin. This inhibition is comparable to the drug concentration needed to inhibit bacterial growth on plates. No loss of activity was observed when a similar concentration of dihydrobicyclomycin was used in place of bicyclomycin, while use of 10-fold higher concentrations of this derivative led to partial rho inhibition. PolyC-dependent ATPase activity from partially purified rho isolated from the mutant BCMr108 was not inhibited by bicyclomycin at concentrations (200 microM) found to completely inhibit wild-type rho. These cumulative findings are consistent with the notion that bicyclomycin expresses its activity by interfering with the polyC-dependent ATPase activity of rho.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8466900 PubMed]

|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

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{{LitMaterials}}

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

{| id="F4e9d99c316af3" 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=63ce1649aab8b3180235b0af7618f667.180716.F4e9d99c316af3&page=180716&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

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

PMID:8466900

2011-10-18T15:22:43Z

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PMID:16181146

2011-10-18T15:22:34Z

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<protect>
 '''Kohn, H and Widger, W''' (2005) The molecular basis for the mode of action of bicyclomycin.''Curr Drug Targets Infect Disord'' '''5''':273-95

{|{{Prettytable}} align = 'center' width= '70%'
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|{{TableHeadingColor}} |'''Abstract''' || <protect>Bicyclomycin (1) is a clinically useful antibiotic exhibiting activity against a broad spectrum of Gram-negative bacteria and against the Gram-positive bacterium, Micrococcus luteus. Bicyclomycin has been used to treat diarrhea in humans and bacterial diarrhea in calves and pigs and is marketed by Fujisawa (Osaka, Japan) under the trade name Bicozamycin. The structure of 1 is unique among antibiotics, and our studies document that its mechanism of action is novel. Early mechanistic proposals suggested that 1 reacted with nucleophiles (e.g., a protein sulfhydryl group) necessary for the remodeling the peptidoglycan assembly within the bacterial cell wall. We, however, showed that 1 targeted the rho transcription termination factor in Escherichia coli. The rho protein is integral to the expression of many gene products in E. coli and other Gram-negative bacteria, and without rho the cell losses viability. Rho is a member of the RecA-type ATPase class of enzymes that use nucleotide contacts to couple oligonucleotide translocation to ATP hydrolysis. Bicyclomycin is the only known selective inhibitor of rho. In this article, we integrate the evidence obtained from bicyclomycin structure-activity studies, site-directed mutagenesis investigations, bicyclomycin affinity labels, and biochemical and biophysical measurements with recent X-ray crystallographic images of the bicyclomycin-rho complex to define the rho antibiotic binding site and to document the pathway for rho inhibition by 1. Together, the structural and functional studies demonstrate how 1, a modest rho inhibitor, can disrupt the rho molecular machinery thereby leading to a catastrophic effect caused by the untimely overproduction of proteins not normally expressed constitutively, thus leading to a toxic effect on the cells.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16181146 PubMed]

|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

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{{LitMaterials}}

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<protect>

{| id="V4e9d99ba82c43" 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=63ce1649aab8b3180235b0af7618f667.180715.V4e9d99ba82c43&page=180715&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
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<references/>

PMID:16181146

2011-10-18T15:22:34Z

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PMID:6297458

2011-10-04T23:25:31Z

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<protect>
 '''Cammack, R, Jackson, RH, Cornish-Bowden, A and Cole, JA''' (1982) Electron-spin-resonance studies of the NADH-dependent nitrite reductase from Escherichia coli K12.''Biochem. J.'' '''207''':333-9

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>The NADH-dependent nitrite reductase of Escherichia coli, which contains sirohaem, flavin, non-haem iron and labile sulphide, was examined by low-temperature e.s.r. spectroscopy. The enzyme, stored in the presence of nitrite and ascorbate, gave the spectrum of a nitrosyl derivative, with hyperfine splitting due to the nitrosyl nitrogen. On removal of these reagents, a series of signals centred around g = 6 was observed, typical of high-spin ferric haem. Cyanide converted this into a low-spin form. On reduction of the enzyme with NADH, an axial spectrum at g = 1.92, 2.01 was observed. The temperature-dependence of this signal is indicative of a [2Fe-2S] iron-sulphur cluster. The midpoint potential of this cluster was estimated to be -230 +/- 15 mV by two independent methods. Reduction of the enzyme with dithionite yielded further signals, which are at present unidentified, at g = 2.1-2.28. No signals were observed that could be assigned to a [4Fe-4S] cluster, such as is found in other sulphite reductases and nitrite reductases that contain sirohaem.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=6297458 PubMed]

|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

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

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<protect>

{| id="T4e8b95eb1fe79" 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=63ce1649aab8b3180235b0af7618f667.180705.T4e8b95eb1fe79&page=180705&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

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==References==
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<references/>

PMID:6297458

2011-10-04T23:25:30Z

165.91.108.111: New PMID: Page!

PMID:3010044

2011-09-14T16:09:43Z

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<protect>
 '''Nara, F, Matsuyama, S, Mizuno, T and Mizushima, S''' (1986) Molecular analysis of mutant ompR genes exhibiting different phenotypes as to osmoregulation of the ompF and ompC genes of Escherichia coli.''Mol. Gen. Genet.'' '''202''':194-9

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>Expression of the ompF and ompC genes coding for major outer membrane proteins is osmoregulated by solutes, such as sucrose and NaCl, in the growth medium. The OmpR protein, a positive regulator of these genes, is involved in the osmoregulation (Dairi et al. 1985; Nara et al. 1984). In the present work, five mutant ompR genes exhibiting different phenotypes of osmoregulation were cloned and sequenced. Three of them, ompR1, ompR2 and ompR20, were previously isolated mutants. The others, ompR3 and ompR4, were isolated in the present work. The ompR1 mutation resulted in the deletion of 19 amino acids near the C-terminus of the OmpR protein. The ompR3 and ompR4 mutations resulted in Arg15 to Cys and Arg71 to Thr conversions, respectively, at the N-terminal portion, whereas the ompR20 and ompR2 mutations resulted in Arg150 to Cys and Val207 to Met conversions, respectively, at the C-terminal portion. Based on these results, the structure and function of the OmpR protein are discussed in relation to the mechanism of osmoregulation.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3010044 PubMed]

|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

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{{LitMaterials}}

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<protect>

{| id="I4e70d1c6c705f" 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=63ce1649aab8b3180235b0af7618f667.180677.I4e70d1c6c705f&page=180677&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
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{{RefHelp}}
<references/>

PMID:3010044

2011-09-14T16:09:42Z

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PMID:16859555

2011-09-07T20:14:58Z

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<protect>
 '''Collins, SR, Schuldiner, M, Krogan, NJ and Weissman, JS''' (2006) A strategy for extracting and analyzing large-scale quantitative epistatic interaction data.''Genome Biol.'' '''7''':R63

{|{{Prettytable}} align = 'center' width= '70%'
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|{{TableHeadingColor}} |'''Abstract''' || <protect>Recently, approaches have been developed for high-throughput identification of synthetic sick/lethal gene pairs. However, these are only a specific example of the broader phenomenon of epistasis, wherein the presence of one mutation modulates the phenotype of another. We present analysis techniques for generating high-confidence quantitative epistasis scores from measurements made using synthetic genetic array and epistatic miniarray profile (E-MAP) technology, as well as several tools for higher-level analysis of the resulting data that are greatly enhanced by the quantitative score and detection of alleviating interactions.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16859555 PubMed]
Online version:[http://dx.doi.org/10.1186/gb-2006-7-7-r63 10.1186/gb-2006-7-7-r63]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

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{{LitMaterials}}

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<protect>

{| id="S4e67d0c257bcc" 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=63ce1649aab8b3180235b0af7618f667.180641.S4e67d0c257bcc&page=180641&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

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<references/>

PMID:16859555

2011-09-07T20:14:57Z

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PMID:2828640

2011-08-09T23:49:35Z

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<protect>
 '''Redfield, RJ and Campbell, AM''' (1987) Structure of cryptic lambda prophages.''J. Mol. Biol.'' '''198''':393-404

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>When Escherichia coli cells lysogenic for bacteriophage lambda are induced with ultraviolet light, cells carrying cryptic lambda prophages are occasionally found among the apparently cured survivors. The lambda variant crypticogen (lambda crg) carries an insertion of the transposable element IS2, which increases the frequency of cryptic lysogens to about 50% of cured cells: 43 of these cryptic prophages have been characterized. They all contain substitutions that replace the early segment of the prophage genome (from the IS2 to near the cos site) with a duplicate copy of a large segment of the host chromosome. The right end of the substitution always results from recombination between the nin-QSR-cos region of the prophage and the homologous incomplete lambdoid prophage Qsr' at 12.5 minutes in the E. coli chromosome. The left end of the substitution is usually a crossover that recombines the IS2 element in the prophage with an E. coli IS2 at 8.5 minutes, near the lac gene, or with a second IS2 located counterclockwise from leu at 2 minutes, generating duplications of at least 200,000 bases. Five cryptic lysogens derived from cells lysogenic for a reference strain of lambda (which lacks the IS2 present in lambda crg) have been characterized. They contain substitutions whose right termini are generated by a crossover with the Qsr' prophage. The left termini of these substitutions are formed either by a crossover between the lambda exo gene and a short exo-homologous segment of Qsr' (2/5), or by a crossover between sequences to the left of attL and an unmapped distant region of the host chromosome (3/5). The large duplications carried by these cryptic lysogens are stable, unlike tandem duplications, and so may significantly influence the cell's evolutionary potential.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=2828640 PubMed]

|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

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{{LitMaterials}}

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<protect>

{| id="B4e41c78f0f609" 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=63ce1649aab8b3180235b0af7618f667.179601.B4e41c78f0f609&page=179601&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

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<references/>

PMID:2828640

2011-08-09T23:49:35Z

165.91.108.111: New PMID: Page!

PMID:21398484

2011-08-09T23:47:54Z

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<protect>
 '''Shen, CR, Lan, EI, Dekishima, Y, Baez, A, Cho, KM and Liao, JC''' (2011) Driving forces enable high-titer anaerobic 1-butanol synthesis in Escherichia coli.''Appl. Environ. Microbiol.'' '''77''':2905-15

{|{{Prettytable}} align = 'center' width= '70%'
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|{{TableHeadingColor}} |'''Abstract''' || <protect>1-Butanol, an important chemical feedstock and advanced biofuel, is produced by Clostridium species. Various efforts have been made to transfer the clostridial 1-butanol pathway into other microorganisms. However, in contrast to similar compounds, only limited titers of 1-butanol were attained. In this work, we constructed a modified clostridial 1-butanol pathway in Escherichia coli to provide an irreversible reaction catalyzed by trans-enoyl-coenzyme A (CoA) reductase (Ter) and created NADH and acetyl-CoA driving forces to direct the flux. We achieved high-titer (30 g/liter) and high-yield (70 to 88% of the theoretical) production of 1-butanol anaerobically, comparable to or exceeding the levels demonstrated by native producers. Without the NADH and acetyl-CoA driving forces, the Ter reaction alone only achieved about 1/10 the level of production. The engineered host platform also enables the selection of essential enzymes with better catalytic efficiency or expression by anaerobic growth rescue. These results demonstrate the importance of driving forces in the efficient production of nonnative products.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=21398484 PubMed]
Online version:[http://dx.doi.org/10.1128/AEM.03034-10 10.1128/AEM.03034-10]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

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{{LitMaterials}}

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<protect>

{| id="N4e41c72a504d6" 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=63ce1649aab8b3180235b0af7618f667.179600.N4e41c72a504d6&page=179600&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

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<references/>

PMID:21398484

2011-08-09T23:47:54Z

165.91.108.111: New PMID: Page!

PMID:21398557

2011-08-09T23:47:36Z

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<protect>
 '''Chubiz, LM and Rao, CV''' (2011) Role of the mar-sox-rob regulon in regulating outer membrane porin expression.''J. Bacteriol.'' '''193''':2252-60

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>Multiple factors control the expression of the outer membrane porins OmpF and OmpC in Escherichia coli. In this work, we investigated the role of the mar-sox-rob regulon in regulating outer membrane porin expression in response to salicylate. We provide both genetic and physiological evidence that MarA and Rob can independently activate micF transcription in response to salicylate, leading to reduced OmpF expression. MarA was also found to repress OmpF expression through a MicF-independent pathway. In the case of OmpC, we found that its transcription was moderately increased in response to salicylate. However, this increase was independent of MarA and Rob. Finally, we found that the reduction in OmpF expression in a tolC mutant is due primarily to Rob. Collectively, this work further clarifies the coordinated role of MarA and Rob in regulating the expression of the outer membrane porins.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=21398557 PubMed]
Online version:[http://dx.doi.org/10.1128/JB.01382-10 10.1128/JB.01382-10]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

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{{LitMaterials}}

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<protect>

{| id="Y4e41c7180eeea" 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=63ce1649aab8b3180235b0af7618f667.179599.Y4e41c7180eeea&page=179599&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

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<references/>

PMID:21398557

2011-08-09T23:47:35Z

165.91.108.111: New PMID: Page!

PMID:21401071

2011-08-09T23:47:18Z

165.91.108.111: Fill PMID: Page!

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<protect>
 '''Imhof, N, Kuhn, A and Gerken, U''' (2011) Substrate-dependent conformational dynamics of the Escherichia coli membrane insertase YidC.''Biochemistry'' '''50''':3229-39

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>The binding of Pf3 coat protein to the membrane insertase YidC from Escherichia coli induces a conformational change in the tertiary structure of the insertase, resulting in a quenching of the intrinsic tryptophan (Trp) fluorescence. Tryptophan mutants of YidC were generated to examine such conformational movements in detail with time-resolved and steady-state fluorescence spectroscopy. Ten of the 11 Trp residues within YidC were substituted to phenylalanines generating single Trp mutants either at position 354, 454, or 508. In addition, a double mutant with Trp residues at 332 and 334 was studied. Purified YidC mutants were reconstituted into DOPC/DOPG vesicles and titrated with a Trp-free mutant of Pf3 coat, enabling a detailed conformational study of the periplasmic P1, P2, and P3 domains of YidC before and after binding of substrate. Time-resolved fluorescence anisotropy revealed that the mobility of the residues W332/W334 and W508 was considerably increased after binding of Pf3 coat to the insertase. Furthermore, analysis of the fluorescence emission spectra and the decay times showed that all Trp residues are embedded in an equivalent environment that is a membrane/water interface.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=21401071 PubMed]
Online version:[http://dx.doi.org/10.1021/bi1020293 10.1021/bi1020293]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

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{{LitMaterials}}

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<protect>

{| id="M4e41c706843a7" 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=63ce1649aab8b3180235b0af7618f667.179598.M4e41c706843a7&page=179598&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

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<references/>

PMID:21401071

2011-08-09T23:47:18Z

165.91.108.111: New PMID: Page!