Hfq links translation repression to stress-induced mutagenesis in E. coli.

ABSTRACT: Mismatch repair (MMR) is a conserved mechanism exploited by cells to correct DNA replication errors both in growing cells and under nongrowing conditions. Hfq (host factor for RNA bacteriophage Qβ replication), a bacterial Lsm family RNA-binding protein, chaperones RNA-RNA interactions between regulatory small RNAs (sRNAs) and target messenger RNAs (mRNAs), leading to alterations of mRNA translation and/or stability. Hfq has been reported to post-transcriptionally repress the DNA MMR gene mutS in stationary phase, possibly limiting MMR to allow increased mutagenesis. Here we report that Hfq deploys dual mechanisms to control mutS expression. First, Hfq binds directly to an (AAN)₃ motif within the mutS 5' untranslated region (UTR), repressing translation in t

SUBMITTER: Chen J 

PROVIDER: S-EPMC5580658 | biostudies-literature | 2017 Jul

REPOSITORIES: biostudies-literature