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Regulation of the general stress response transcription factor RpoS by small, non‐coding RNAs
Author(s) -
McCullen Colleen A,
Benhammou Jihane,
Gottesman Susan
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.lb31
Subject(s) - rpos , biology , messenger rna , transcription (linguistics) , genetics , untranslated region , rnase p , translation (biology) , sigma factor , gene expression , microbiology and biotechnology , rna , gene , promoter , linguistics , philosophy
Small, non‐coding RNAs (sRNAs) positively and negatively regulate gene expression in Escherichia coli by base pairing with mRNAs and modulating translation and/or mRNA stability. The sRNAs DsrA and RprA stimulate the synthesis of the stress response transcription factor RpoS by base pairing with the 5′ untranslated region of the rpoS mRNA. We hypothesized that sRNA pairing in this region acts to stabilize the mRNA. Northern blot analysis demonstrated that rpoS mRNA was unstable in the absence of these sRNAs and expression of DsrA or RprA stabilized this mRNA. Mutations in the sRNAs or in rpoS that disrupt base pairing blocked this stabilizing effect. We also found that the endoribonuclease RNaseE degraded rpoS mRNA and that pairing with DsrA was no longer required for rpoS mRNA stability in an RNaseE mutant strain. However, DsrA was required for maximal translation of RpoS. This suggests that DsrA protects rpoS mRNA from degradation by RNaseE and that DsrA has a further activity in stimulating RpoS protein synthesis. In contrast, RNaseIII degraded the rpoS mRNA in the presence and absence of DsrA, limiting the translation of rpoS mRNA. This latter data suggests that RNase III plays a role in negatively regulating RpoS synthesis in this context. This work is supported by National Institutes of Health grant F32 GM075392 and the National Cancer Institute intramural research program.