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Messenger RNA interferase RelE controls relBE transcription by conditional cooperativity

Lookup NU author(s): Professor Kenn Gerdes

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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 neutralizes 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 as a 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. In 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 RelB2·RelE complexes to the operator sites. Thus, RelE controls relBE transcription by conditional cooperativity. © 2008 The Authors.

Publication metadata

Author(s): Overgaard M, Borch J, Jørgensen MG, Gerdes K

Publication type: Article

Publication status: Published

Journal: Molecular Microbiology

Year: 2008

Volume: 69

Issue: 4

Pages: 841-857

ISSN (print): 0950-382X

ISSN (electronic): 1365-2958

Publisher: Wiley-Blackwell Publishing Ltd.

URL: http://dx.doi.org/10.1111/j.1365-2958.2008.06313.x

DOI: 10.1111/j.1365-2958.2008.06313.x

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