Double locking of an Escherichia coli promoter by two repressors prevents premature colicin expression and cell lysis

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Double locking of an Escherichia coli promoter by two repressors prevents premature colicin expression and cell lysis. / Butala, Matej; Sonjak, Silva; Kamenšek, Simona; Hodošček, Milan; Browning, Douglas F; Žgur-Bertok, Darja; Busby, Stephen J W.

In: Molecular Microbiology, Vol. 86, No. 1, 2012, p. 129-39.

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@article{854b4343dab84971b78de7763774e036,
title = "Double locking of an Escherichia coli promoter by two repressors prevents premature colicin expression and cell lysis",
abstract = "The synthesis of Eschericha coli colicins is lethal to the producing cell and is repressed during normal growth by the LexA transcription factor, which is the master repressor of the SOS system for repair of DNA damage. Following DNA damage, LexA is inactivated and SOS repair genes are induced immediately, but colicin production is delayed and induced only in terminally damaged cells. The cause of this delay is unknown. Here we identify the global transcription repressor, IscR, as being directly responsible for the delay in colicin K expression during the SOS response, and identify the DNA target for IscR at the colicin K operon promoter. Our results suggest that, IscR stabilizes LexA at the cka promoter after DNA damage thus, preventing its cleavage and inactivation, and this cooperation ensures that suicidal colicin K production is switched on only as a last resort. A similar mechanism operates at the regulatory region of other colicins and, hence, we suggest that many promoters that control the expression of 'lethal' genes are double locked.",
author = "Matej Butala and Silva Sonjak and Simona Kamen{\v s}ek and Milan Hodo{\v s}{\v c}ek and Browning, {Douglas F} and Darja {\v Z}gur-Bertok and Busby, {Stephen J W}",
note = "{\textcopyright} 2012 Blackwell Publishing Ltd.",
year = "2012",
doi = "10.1111/j.1365-2958.2012.08179.x",
language = "English",
volume = "86",
pages = "129--39",
journal = "Molecular Microbiology",
issn = "0950-382X",
publisher = "Wiley",
number = "1",

}

RIS

TY - JOUR

T1 - Double locking of an Escherichia coli promoter by two repressors prevents premature colicin expression and cell lysis

AU - Butala, Matej

AU - Sonjak, Silva

AU - Kamenšek, Simona

AU - Hodošček, Milan

AU - Browning, Douglas F

AU - Žgur-Bertok, Darja

AU - Busby, Stephen J W

N1 - © 2012 Blackwell Publishing Ltd.

PY - 2012

Y1 - 2012

N2 - The synthesis of Eschericha coli colicins is lethal to the producing cell and is repressed during normal growth by the LexA transcription factor, which is the master repressor of the SOS system for repair of DNA damage. Following DNA damage, LexA is inactivated and SOS repair genes are induced immediately, but colicin production is delayed and induced only in terminally damaged cells. The cause of this delay is unknown. Here we identify the global transcription repressor, IscR, as being directly responsible for the delay in colicin K expression during the SOS response, and identify the DNA target for IscR at the colicin K operon promoter. Our results suggest that, IscR stabilizes LexA at the cka promoter after DNA damage thus, preventing its cleavage and inactivation, and this cooperation ensures that suicidal colicin K production is switched on only as a last resort. A similar mechanism operates at the regulatory region of other colicins and, hence, we suggest that many promoters that control the expression of 'lethal' genes are double locked.

AB - The synthesis of Eschericha coli colicins is lethal to the producing cell and is repressed during normal growth by the LexA transcription factor, which is the master repressor of the SOS system for repair of DNA damage. Following DNA damage, LexA is inactivated and SOS repair genes are induced immediately, but colicin production is delayed and induced only in terminally damaged cells. The cause of this delay is unknown. Here we identify the global transcription repressor, IscR, as being directly responsible for the delay in colicin K expression during the SOS response, and identify the DNA target for IscR at the colicin K operon promoter. Our results suggest that, IscR stabilizes LexA at the cka promoter after DNA damage thus, preventing its cleavage and inactivation, and this cooperation ensures that suicidal colicin K production is switched on only as a last resort. A similar mechanism operates at the regulatory region of other colicins and, hence, we suggest that many promoters that control the expression of 'lethal' genes are double locked.

U2 - 10.1111/j.1365-2958.2012.08179.x

DO - 10.1111/j.1365-2958.2012.08179.x

M3 - Article

C2 - 22812562

VL - 86

SP - 129

EP - 139

JO - Molecular Microbiology

JF - Molecular Microbiology

SN - 0950-382X

IS - 1

ER -