Overexpression of the LexA-regulated tisAB RNA in E. coli inhibits SOS functions; implications for regulation of the SOS response.

2.50
Hdl Handle:
http://hdl.handle.net/10143/67433
Title:
Overexpression of the LexA-regulated tisAB RNA in E. coli inhibits SOS functions; implications for regulation of the SOS response.
Authors:
Weel-Sneve, Ragnhild; Bjørås, Magnar; Kristiansen, Knut Ivan
Citation:
Nucleic acids research 2008, 36 (19):6249-59
Additional Links:
http://nar.oxfordjournals.org/cgi/content/full/36/19/6249

Full metadata record

DC FieldValue Language
dc.contributor.authorWeel-Sneve, Ragnhild-
dc.contributor.authorBjørås, Magnar-
dc.contributor.authorKristiansen, Knut Ivan-
dc.date.accessioned2009-05-07T07:11:53Z-
dc.date.available2009-05-07T07:11:53Z-
dc.date.issued2008-11-
dc.identifier.citationNucleic acids research 2008, 36 (19):6249-59en
dc.identifier.issn1362-4962-
dc.identifier.pmid18832374-
dc.identifier.doi10.1093/nar/gkn633-
dc.identifier.urihttp://hdl.handle.net/10143/67433-
dc.description.abstractThe DNA damage induced SOS response in Escherichia coli is initiated by cleavage of the LexA repressor through activation of RecA. Here we demonstrate that overexpression of the SOS-inducible tisAB gene inhibits several SOS functions in vivo. Wild-type E. coli overexpressing tisAB showed the same UV sensitivity as a lexA mutant carrying a noncleavable version of the LexA protein unable to induce the SOS response. Immunoblotting confirmed that tisAB overexpression leads to higher levels of LexA repressor and northern experiments demonstrated delayed and reduced induction of recA mRNA. In addition, induction of prophage lambda and UV-induced filamentation was inhibited by tisAB overexpression. The tisAB gene contains antisense sequences to the SOS-inducible dinD gene (16 nt) and the uxaA gene (20 nt), the latter encoding a dehydratase essential for galacturonate catabolism. Cleavage of uxaA mRNA at the antisense sequence was dependent on tisAB RNA expression. We showed that overexpression of tisAB is less able to confer UV sensitivity to the uxaA dinD double mutant as compared to wild-type, indicating that the dinD and uxaA transcripts modulate the anti-SOS response of tisAB. These data shed new light on the complexity of SOS regulation in which the uxaA gene could link sugar metabolism to the SOS response via antisense regulation of the tisAB gene.en
dc.language.isoenen
dc.relation.urlhttp://nar.oxfordjournals.org/cgi/content/full/36/19/6249en
dc.subjectNevrologien
dc.subject.meshAmino Acid Sequenceen
dc.subject.meshBacterial Proteinsen
dc.subject.meshBacteriophage lambdaen
dc.subject.meshBase Sequenceen
dc.subject.meshEscherichia colien
dc.subject.meshEscherichia coli Proteinsen
dc.subject.meshGene Expression Regulation, Bacterialen
dc.subject.meshMolecular Sequence Dataen
dc.subject.meshMutagenesisen
dc.subject.meshOpen Reading Framesen
dc.subject.meshPlasmidsen
dc.subject.meshProphagesen
dc.subject.meshRNA, Antisenseen
dc.subject.meshRNA, Messengeren
dc.subject.meshRec A Recombinasesen
dc.subject.meshRepressor Proteinsen
dc.subject.meshSOS Response (Genetics)en
dc.subject.meshSerine Endopeptidasesen
dc.subject.meshUltraviolet Raysen
dc.titleOverexpression of the LexA-regulated tisAB RNA in E. coli inhibits SOS functions; implications for regulation of the SOS response.en
dc.typeJournal articleen
dc.typepeer revieweden
dc.contributor.departmentCentre for Molecular Biology and Neuroscience, Institute of Medical Microbiology, Rikshospitalet University Hospital, NO-0027 Oslo, Norway.en
dc.identifier.journalNucleic acids researchen
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