Messenger RNA Interferase RelE Controls relBE Transcription by Conditional Cooperativity

Martin Overgaard, Jonas Borch, Mikkel G Jørgensen, Kenn Gerdes

Research output: Contribution to journalJournal articleResearchpeer-review

Abstract

Prokaryotic toxin-antitoxin (TA) loci consist of two genes in an operon that encodes a metabolically stable toxin and an unstable antitoxin. The antitoxin neutralises its cognate toxin by forming a tight complex with it. In all cases known, the antitoxin autoregulates TA operon transcription by binding to one or more operators in the promoter region while the toxin functions as a co-repressor of transcription. Interestingly, the toxin can also stimulate TA operon transcription. Here we analyse mechanistic aspects of how RelE of Escherichia coli can function both as a co-repressor and derepressor of relBE transcription. When RelB was in excess to RelE, two trimeric RelB(2)*RelE complexes bound cooperatively to two adjacent operator-sites in the relBE promoter region and repressed transcription. By contrast, RelE in excess stimulated relBE transcription and released the RelB(2)*RelE complex from operator DNA. A mutational analysis of the operator-sites showed that RelE in excess counteracted cooperative binding of the RelB(2)*RelE complexes to the operator-sites. Thus, RelE controls relBE transcription by conditional cooperativity.
Original languageEnglish
JournalMolecular Microbiology
Volume69
Issue number4
Pages (from-to)841-857
Number of pages16
ISSN0950-382X
DOIs
Publication statusPublished - 2008

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