EcoliWiki - User contributions [en]

PMID:20668389

2010-09-21T18:31:02Z

193.49.235.4: Fill PMID: Page!

{{RightTOC}}
<protect>
 '''Pennetier, C, Oberto, J and Plumbridge, J''' (2010) An antisense transcript from within the ptsG promoter region in Escherichia coli.''J. Mol. Microbiol. Biotechnol.'' '''18''':230-40

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>The ptsG gene, encoding the major glucose uptake system in Escherichia coli, is expressed from 2 promoters, a minor promoter p2 and a major downstream promoter p1. Transcription from both promoters is repressed by Mlc, and expression of p1 is activated by the cAMP/catabolite activator protein complex. Expression from p1 is also regulated post-transcriptionally in response to sugar stress via an sRNA, SgrS, which results in translational inhibition and mRNA degradation. Here, we demonstrate an additional level of complexity to the transcriptional pattern surrounding ptsG. A third promoter, p3, located between p1 and p2, was found to express a transcript antisense to ptsG. This promoter was detected by in vitro transcription and by RNA polymerase footprinting techniques and in vivo by S1 analysis and fusions with a lacZ reporter gene. Although the intrinsic strength of the p3 promoter was comparable to that of ptsG, it proved difficult to identify a full-length transcript. A faint transcript of greater than 400 nt could be detected. The transcript thus has more of the characteristics of a divergently expressed cryptic unstable transcript (CUT) than a prokaryotic sRNA.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' ||
* [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=20668389 PubMed]
Online version:[http://dx.doi.org/10.1159/000319598 10.1159/000319598]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

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

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

{| id="F4c98f9e687c90" 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=63ce1649aab8b3180235b0af7618f667.176145.F4c98f9e687c90&page=176145&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

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

==See also==

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

PMID:20668389

2010-09-21T18:31:02Z

193.49.235.4: New PMID: Page!

PMID:20167073

2010-04-14T15:12:17Z

193.49.235.4: Fill PMID: Page!

{{RightTOC}}
<protect>
 '''Le Derout, J, Boni, IV, Régnier, P and Hajnsdorf, E''' (2010) Hfq affects mRNA levels independently of degradation.''BMC Mol. Biol.'' '''11''':17

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>BACKGROUND: The bacterial Lsm protein, Hfq, is an RNA chaperone involved in many reactions related to RNA metabolism, such as replication and stability, control of small RNA activity and polyadenylation. Despite this wide spectrum of known functions, the global role of Hfq is almost certainly undervalued; its capacity to bind DNA and to interact with many other proteins are only now beginning to be taken into account. RESULTS: The role of Hfq in the maturation and degradation of the rpsO mRNA of E. coli was investigated in vivo. The data revealed a decrease in rpsO mRNA abundance concomitant to an increase in its stability when Hfq is absent. This indicates that the change in mRNA levels in hfq mutants does not result from its modification of RNA stability. Moreover, a series of independent experiments have revealed that the decrease in mRNA level is not a consequence of a reduction of translation efficiency and that Hfq is not directly implicated in translational control of rpsO expression. Reduced steady-state mRNA levels in the absence of Hfq were also shown for rpsT, rpsB and rpsB-tsf, but not for lpp, pnp or tRNA transcripts. The abundance of chimeric transcripts rpsO-lacZ and rpsB-lacZ, whose expression was driven by rpsO and rpsB promoters, respectively, was also lower in the hfq null-mutants, while the beta-galactosidase yield remained about the same as in the parent wild-type strain. CONCLUSIONS: The data obtained suggest that alteration of rpsO, rpsT and rpsB-tsf transcript levels observed under conditions of Hfq deficiency is not caused by the post-transcriptional events, such as mRNA destabilization or changes in translation control, and may rather result from changes in transcriptional activity. So far, how Hfq affects transcription remains unclear. We propose that one of the likely mechanisms of Hfq-mediated modulation of transcription might operate early in the elongation step, when interaction of Hfq with a nascent transcript would help to overcome transcription pauses and to prevent preliminary transcript release.</protect>
|-
|{{TableHeadingColor}} nowrap |'''Links''' || [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=20167073 PubMed] Online version:[http://dx.doi.org/10.1186/1471-2199-11-17 10.1186/1471-2199-11-17]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

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

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

{| id="I4bc5db518460f" 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=63ce1649aab8b3180235b0af7618f667.171756.I4bc5db518460f&page=171756&pagename={{FULLPAGENAMEE}}&type=0&template=GO_table_reference edit table] || || || || || || || ||
|}
</protect>

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

==See also==

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

PMID:20167073

2010-04-14T15:12:17Z

193.49.235.4: New PMID: Page!