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Sigma E controls biogenesis of the antisense RNA MicA.

Udekwu KI, Wagner EG - Nucleic Acids Res. (2007)

Bottom Line: This regulation is Hfq-dependent and occurs by MicA-dependent translational inhibition which facilitates mRNA decay.Such treatments are sensed as envelope stress, upon which the extracytoplasmic sigma factor sigma(E) is activated.The strict dependence of micA transcription on sigma(E) is supported by three observations.

View Article: PubMed Central - PubMed

Affiliation: Department of Cell & Molecular Biology, Uppsala university, Biomedical Center, Box 596, S-75124 Uppsala, Sweden. klas.udekwu@icm.uu.se

ABSTRACT
Adaptation stress responses in the Gram-negative bacterium Escherichia coli and its relatives involve a growing list of small regulatory RNAs (sRNAs). Previous work by us and others showed that the antisense RNA MicA downregulates the synthesis of the outer membrane protein OmpA upon entry into stationary phase. This regulation is Hfq-dependent and occurs by MicA-dependent translational inhibition which facilitates mRNA decay. In this article, we investigate the transcriptional regulation of the micA gene. Induction of MicA is dependent on the alarmone ppGpp, suggestive of alternative sigma factor involvement, yet MicA accumulates in the absence of the general stress/stationary phase sigma(S). We identified stress conditions that induce high MicA levels even during exponential growth-a phase in which MicA levels are low (ethanol, hyperosmolarity and heat shock). Such treatments are sensed as envelope stress, upon which the extracytoplasmic sigma factor sigma(E) is activated. The strict dependence of micA transcription on sigma(E) is supported by three observations. Induced overexpression of sigma(E) increases micA transcription, an DeltarpoE mutant displays undetectable MicA levels and the micA promoter has the consensus sigma(E) signature. Thus, MicA is part of the sigma(E) regulon and downregulates its target gene, ompA, probably to alleviate membrane stress.

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Conservation of σE recognition motifs in the micA promoter. Alignment of the micA promoter regions from several enterobacteria. Shaded boxes show regions of 100% sequence conservation. The positions of the −35 and −10 boxes, and of the transcription start site (+1), are shown. The invariable C residue in the −10 box is highlighted. An AT-rich element is present upstream of the −35 box. The consensus sequence of a σE-dependent promoter (14) is shown for comparison. Accession numbers of aligned sequences: E. coli U00096.2; Salmonella typhi AL627276.1; Serratia marcescens AJ628150.1; Shigella flexneri AE005674.1; Yersinia pestis AE017128.1.
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Figure 3: Conservation of σE recognition motifs in the micA promoter. Alignment of the micA promoter regions from several enterobacteria. Shaded boxes show regions of 100% sequence conservation. The positions of the −35 and −10 boxes, and of the transcription start site (+1), are shown. The invariable C residue in the −10 box is highlighted. An AT-rich element is present upstream of the −35 box. The consensus sequence of a σE-dependent promoter (14) is shown for comparison. Accession numbers of aligned sequences: E. coli U00096.2; Salmonella typhi AL627276.1; Serratia marcescens AJ628150.1; Shigella flexneri AE005674.1; Yersinia pestis AE017128.1.

Mentions: Selected micA upstream sequences from several enterobacterial genomes (gamma proteobacteriaceae subdivision) were aligned. We aligned the sequence ranging from the known E. coli micA gene −55 to +4 sequence (+1 being the transcription start site (8; K.U., unpublished)) with corresponding regions in related genomes. Alignment to the consensus rpoE recognition module was based on previous research (14,19). Sequences were obtained from the NCBI database, and BLAST (http://www.ncbi.nlm.nih.gov/BLAST) and accession numbers indicated are listed in the Figure 3 legend.Figure 1.


Sigma E controls biogenesis of the antisense RNA MicA.

Udekwu KI, Wagner EG - Nucleic Acids Res. (2007)

Conservation of σE recognition motifs in the micA promoter. Alignment of the micA promoter regions from several enterobacteria. Shaded boxes show regions of 100% sequence conservation. The positions of the −35 and −10 boxes, and of the transcription start site (+1), are shown. The invariable C residue in the −10 box is highlighted. An AT-rich element is present upstream of the −35 box. The consensus sequence of a σE-dependent promoter (14) is shown for comparison. Accession numbers of aligned sequences: E. coli U00096.2; Salmonella typhi AL627276.1; Serratia marcescens AJ628150.1; Shigella flexneri AE005674.1; Yersinia pestis AE017128.1.
© Copyright Policy - openaccess
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC1851643&req=5

Figure 3: Conservation of σE recognition motifs in the micA promoter. Alignment of the micA promoter regions from several enterobacteria. Shaded boxes show regions of 100% sequence conservation. The positions of the −35 and −10 boxes, and of the transcription start site (+1), are shown. The invariable C residue in the −10 box is highlighted. An AT-rich element is present upstream of the −35 box. The consensus sequence of a σE-dependent promoter (14) is shown for comparison. Accession numbers of aligned sequences: E. coli U00096.2; Salmonella typhi AL627276.1; Serratia marcescens AJ628150.1; Shigella flexneri AE005674.1; Yersinia pestis AE017128.1.
Mentions: Selected micA upstream sequences from several enterobacterial genomes (gamma proteobacteriaceae subdivision) were aligned. We aligned the sequence ranging from the known E. coli micA gene −55 to +4 sequence (+1 being the transcription start site (8; K.U., unpublished)) with corresponding regions in related genomes. Alignment to the consensus rpoE recognition module was based on previous research (14,19). Sequences were obtained from the NCBI database, and BLAST (http://www.ncbi.nlm.nih.gov/BLAST) and accession numbers indicated are listed in the Figure 3 legend.Figure 1.

Bottom Line: This regulation is Hfq-dependent and occurs by MicA-dependent translational inhibition which facilitates mRNA decay.Such treatments are sensed as envelope stress, upon which the extracytoplasmic sigma factor sigma(E) is activated.The strict dependence of micA transcription on sigma(E) is supported by three observations.

View Article: PubMed Central - PubMed

Affiliation: Department of Cell & Molecular Biology, Uppsala university, Biomedical Center, Box 596, S-75124 Uppsala, Sweden. klas.udekwu@icm.uu.se

ABSTRACT
Adaptation stress responses in the Gram-negative bacterium Escherichia coli and its relatives involve a growing list of small regulatory RNAs (sRNAs). Previous work by us and others showed that the antisense RNA MicA downregulates the synthesis of the outer membrane protein OmpA upon entry into stationary phase. This regulation is Hfq-dependent and occurs by MicA-dependent translational inhibition which facilitates mRNA decay. In this article, we investigate the transcriptional regulation of the micA gene. Induction of MicA is dependent on the alarmone ppGpp, suggestive of alternative sigma factor involvement, yet MicA accumulates in the absence of the general stress/stationary phase sigma(S). We identified stress conditions that induce high MicA levels even during exponential growth-a phase in which MicA levels are low (ethanol, hyperosmolarity and heat shock). Such treatments are sensed as envelope stress, upon which the extracytoplasmic sigma factor sigma(E) is activated. The strict dependence of micA transcription on sigma(E) is supported by three observations. Induced overexpression of sigma(E) increases micA transcription, an DeltarpoE mutant displays undetectable MicA levels and the micA promoter has the consensus sigma(E) signature. Thus, MicA is part of the sigma(E) regulon and downregulates its target gene, ompA, probably to alleviate membrane stress.

Show MeSH
Related in: MedlinePlus