Messenger RNA interferase RelE controls relBE transcription by conditional cooperativity

Martin Overgaard; Jonas Borch; Mikkel G. Jorgensen; Kenn Gerdes

doi:10.1111/j.1365-2958.2008.06313.x

Messenger RNA interferase RelE controls relBE transcription by conditional cooperativity

Martin Overgaard, Jonas Borch, Mikkel G. Jorgensen, Kenn Gerdes

142 Citationer (Scopus)

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 ReIE of Escherichia coli can function both as a co-repressor and as a derepressor of relBE transcription. When ROB was in excess to ReIE, two trimeric ReIB(2)center dot ReIE complexes bound cooperatively to two adjacent operator sites in the reIBE promoter region and repressed transcription. In contrast, ReIE in excess stimulated re/BE transcription and released the ReIB(2)center dot ReIE complex from operator DNA. A mutational analysis of the operator sites showed that ReIE in excess counteracted cooperative binding of the ReIB(2)center dot ReIE complexes to the operator sites. Thus, ReIE controls relBEtranscription by conditional cooperativity.

Originalsprog	Engelsk
Tidsskrift	Molecular Microbiology
Vol/bind	69
Udgave nummer	4
Sider (fra-til)	841-857
Antal sider	17
ISSN	0950-382X
DOI	https://doi.org/10.1111/j.1365-2958.2008.06313.x
Status	Udgivet - 2008
Udgivet eksternt	Ja

Adgang til dokumentet

10.1111/j.1365-2958.2008.06313.x

Citationsformater

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title = "Messenger RNA interferase RelE controls relBE transcription by conditional cooperativity",

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 ReIE of Escherichia coli can function both as a co-repressor and as a derepressor of relBE transcription. When ROB was in excess to ReIE, two trimeric ReIB(2)center dot ReIE complexes bound cooperatively to two adjacent operator sites in the reIBE promoter region and repressed transcription. In contrast, ReIE in excess stimulated re/BE transcription and released the ReIB(2)center dot ReIE complex from operator DNA. A mutational analysis of the operator sites showed that ReIE in excess counteracted cooperative binding of the ReIB(2)center dot ReIE complexes to the operator sites. Thus, ReIE controls relBEtranscription by conditional cooperativity.",

author = "Martin Overgaard and Jonas Borch and Jorgensen, {Mikkel G.} and Kenn Gerdes",

year = "2008",

doi = "10.1111/j.1365-2958.2008.06313.x",

language = "English",

volume = "69",

pages = "841--857",

journal = "Molecular Microbiology",

issn = "0950-382X",

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TY - JOUR

T1 - Messenger RNA interferase RelE controls relBE transcription by conditional cooperativity

AU - Overgaard, Martin

AU - Borch, Jonas

AU - Jorgensen, Mikkel G.

AU - Gerdes, Kenn

PY - 2008

Y1 - 2008

N2 - 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 ReIE of Escherichia coli can function both as a co-repressor and as a derepressor of relBE transcription. When ROB was in excess to ReIE, two trimeric ReIB(2)center dot ReIE complexes bound cooperatively to two adjacent operator sites in the reIBE promoter region and repressed transcription. In contrast, ReIE in excess stimulated re/BE transcription and released the ReIB(2)center dot ReIE complex from operator DNA. A mutational analysis of the operator sites showed that ReIE in excess counteracted cooperative binding of the ReIB(2)center dot ReIE complexes to the operator sites. Thus, ReIE controls relBEtranscription by conditional cooperativity.

AB - 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 ReIE of Escherichia coli can function both as a co-repressor and as a derepressor of relBE transcription. When ROB was in excess to ReIE, two trimeric ReIB(2)center dot ReIE complexes bound cooperatively to two adjacent operator sites in the reIBE promoter region and repressed transcription. In contrast, ReIE in excess stimulated re/BE transcription and released the ReIB(2)center dot ReIE complex from operator DNA. A mutational analysis of the operator sites showed that ReIE in excess counteracted cooperative binding of the ReIB(2)center dot ReIE complexes to the operator sites. Thus, ReIE controls relBEtranscription by conditional cooperativity.

U2 - 10.1111/j.1365-2958.2008.06313.x

DO - 10.1111/j.1365-2958.2008.06313.x

M3 - Journal article

C2 - 18532983

SN - 0950-382X

VL - 69

SP - 841

EP - 857

JO - Molecular Microbiology

JF - Molecular Microbiology

IS - 4

ER -