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