{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T01:56:07Z","timestamp":1773626167675,"version":"3.50.1"},"reference-count":41,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2009,4,14]],"date-time":"2009-04-14T00:00:00Z","timestamp":1239667200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Microbiology"],"published-print":{"date-parts":[[2009,5]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Toxin\u2013antitoxin loci have been identified in almost all free\u2010living prokaryotes, often in high copy numbers. The biological function and molecular targets of the abundant <jats:italic>vapBC<\/jats:italic> loci are not yet known. Here we analyse the <jats:italic>vapBC<\/jats:italic> loci of <jats:italic>Salmonella<\/jats:italic> LT2 and <jats:italic>Shigella<\/jats:italic> plasmid pMYSH6000. Both loci encode putative PIN (<jats:styled-content>Pi<\/jats:styled-content>lT <jats:styled-content>N<\/jats:styled-content>\u2010terminal) domain toxins, and antitoxins that may regulate <jats:italic>vapBC<\/jats:italic> transcription. We show that <jats:italic>vapBC<\/jats:italic><jats:sub>LT2<\/jats:sub> and <jats:italic>vapBC<\/jats:italic><jats:sub>pMYSH<\/jats:sub> are <jats:italic>bona fide<\/jats:italic> TA loci: (i) both VapCs inhibited cell growth very efficiently and were counteracted by the cognate VapBs; (ii) both VapCs inhibited translation; (iii) transcription of the <jats:italic>vapBC<\/jats:italic> loci was induced by amino acid starvation and chloramphenicol, consistent with the proposal that VapB is an unstable inhibitor of <jats:italic>vapBC<\/jats:italic> transcription; (iv) ectopic expression of both VapCs induced a bacteriostatic condition that could be reversed by the cognate antitoxins. Unexpectedly, induction of <jats:italic>vapC<\/jats:italic> in <jats:italic>Escherichia coli<\/jats:italic> resulted in mRNA cleavage at stop\u2010codons. Surprisingly, these cleavages depended on the <jats:italic>yefM yoeB<\/jats:italic> locus, indicating cross\u2010activation between different toxins, that is, VapC activated YoeB mRNA interferase. Activation of YoeB depended on Lon, indicating that Lon degrades YefM antitoxin. Based on these results we present a model that explains activation of YoeB.<\/jats:p>","DOI":"10.1111\/j.1365-2958.2009.06694.x","type":"journal-article","created":{"date-parts":[[2009,4,14]],"date-time":"2009-04-14T06:43:17Z","timestamp":1239691397000},"page":"918-930","source":"Crossref","is-referenced-by-count":62,"title":["Ectopic production of VapCs from <i>Enterobacteria<\/i> inhibits translation and <i>trans<\/i>\u2010activates YoeB mRNA interferase"],"prefix":"10.1111","volume":"72","author":[{"given":"Kristoffer 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