<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>31(13)</volume><submitter>Chen J</submitter><funding>National Cancer Institute</funding><funding>National Institutes of Health</funding><funding>Center for Cancer Research</funding><pubmed_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 &lt;i>mutS&lt;/i> in stationary phase, possibly limiting MMR to allow increased mutagenesis. Here we report that Hfq deploys dual mechanisms to control &lt;i>mutS&lt;/i> expression. First, Hfq binds directly to an (AAN)&lt;sub>3&lt;/sub> motif within the &lt;i>mutS&lt;/i> 5' untranslated region (UTR), repressing translation in t</pubmed_abstract><journal>Genes &amp; development</journal><pagination>1382-1395</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5580658</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Hfq links translation repression to stress-induced mutagenesis in &lt;i>E. coli&lt;/i>.</pubmed_title><pmcid>PMC5580658</pmcid><pubmed_authors>Chen J</pubmed_authors><pubmed_authors>Gottesman S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Hfq links translation repression to stress-induced mutagenesis in &lt;i>E. coli&lt;/i>.</name><description>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 &lt;i>mutS&lt;/i> in stationary phase, possibly limiting MMR to allow increased mutagenesis. Here we report that Hfq deploys dual mechanisms to control &lt;i>mutS&lt;/i> expression. First, Hfq binds directly to an (AAN)&lt;sub>3&lt;/sub> motif within the &lt;i>mutS&lt;/i> 5' untranslated region (UTR), repressing translation in t</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Jul</publication><modification>2025-04-22T03:43:10.403Z</modification><creation>2019-03-27T02:55:11Z</creation></dates><accession>S-EPMC5580658</accession><cross_references><pubmed>28794186</pubmed><doi>10.1101/gad.302547.117</doi></cross_references></HashMap>