Silencing of DNase colicin E8 gene expression by a complex nucleoprotein assembly ensures timely colicin induction

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Silencing of DNase colicin E8 gene expression by a complex nucleoprotein assembly ensures timely colicin induction. / Kamenšek, Simona; Browning, Douglas F.; Podlesek, Zdravko; Busby, Stephen J. W.; Žgur-bertok, Darja; Butala, Matej.

In: PLoS Genetics, Vol. 11, No. 6, e1005354, 26.06.2015.

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@article{6668a03c33d84a06aea6bbfb4c05f653,
title = "Silencing of DNase colicin E8 gene expression by a complex nucleoprotein assembly ensures timely colicin induction",
abstract = "Colicins are plasmid-encoded narrow spectrum antibiotics that are synthesized by strains of Escherichia coli and govern intraspecies competition. In a previous report, we demonstrated that the global transcriptional factor IscR, co dependently with the master regulator of the DNA damage response, LexA, delays induction of the pore forming colicin genes after SOS induction. Here we show that IscR is not involved in the regulation of nuclease colicins, but that the AsnC protein is. We report that AsnC, in concert with LexA, is the key controller of the temporal induction of the DNA degrading colicin E8 gene (cea8), after DNA damage. We demonstrate that a large AsnC nucleosome-like structure, in conjunction with two LexA molecules, prevent cea8 transcription initiation and that AsnC binding activity is directly modulated by L asparagine. We show that L-asparagine is an environmental factor that has a marked impact on cea8 promoter regulation. Our results show that AsnC also modulates the expression of several other DNase and RNase colicin genes but does not substantially affect pore-forming colicin K gene expression. We propose that selection pressure has {"}chosen{"} highly conserved regulators to control colicin expression in E. coli strains, enabling similar colicin gene silencing among bacteria upon exchange of colicinogenic plasmids.",
keywords = "DNA damage, Promoter regions, DNA-binding proteins, Nucleases, Regulator genes, Deoxyribonucleases, Electrophoretic mobility shift assay, Gene expression",
author = "Simona Kamen{\v s}ek and Browning, {Douglas F.} and Zdravko Podlesek and Busby, {Stephen J. W.} and Darja {\v Z}gur-bertok and Matej Butala",
year = "2015",
month = jun,
day = "26",
doi = "10.1371/journal.pgen.1005354",
language = "English",
volume = "11",
journal = "PLoS Genetics",
issn = "1553-7390",
publisher = "Public Library of Science (PLOS)",
number = "6",

}

RIS

TY - JOUR

T1 - Silencing of DNase colicin E8 gene expression by a complex nucleoprotein assembly ensures timely colicin induction

AU - Kamenšek, Simona

AU - Browning, Douglas F.

AU - Podlesek, Zdravko

AU - Busby, Stephen J. W.

AU - Žgur-bertok, Darja

AU - Butala, Matej

PY - 2015/6/26

Y1 - 2015/6/26

N2 - Colicins are plasmid-encoded narrow spectrum antibiotics that are synthesized by strains of Escherichia coli and govern intraspecies competition. In a previous report, we demonstrated that the global transcriptional factor IscR, co dependently with the master regulator of the DNA damage response, LexA, delays induction of the pore forming colicin genes after SOS induction. Here we show that IscR is not involved in the regulation of nuclease colicins, but that the AsnC protein is. We report that AsnC, in concert with LexA, is the key controller of the temporal induction of the DNA degrading colicin E8 gene (cea8), after DNA damage. We demonstrate that a large AsnC nucleosome-like structure, in conjunction with two LexA molecules, prevent cea8 transcription initiation and that AsnC binding activity is directly modulated by L asparagine. We show that L-asparagine is an environmental factor that has a marked impact on cea8 promoter regulation. Our results show that AsnC also modulates the expression of several other DNase and RNase colicin genes but does not substantially affect pore-forming colicin K gene expression. We propose that selection pressure has "chosen" highly conserved regulators to control colicin expression in E. coli strains, enabling similar colicin gene silencing among bacteria upon exchange of colicinogenic plasmids.

AB - Colicins are plasmid-encoded narrow spectrum antibiotics that are synthesized by strains of Escherichia coli and govern intraspecies competition. In a previous report, we demonstrated that the global transcriptional factor IscR, co dependently with the master regulator of the DNA damage response, LexA, delays induction of the pore forming colicin genes after SOS induction. Here we show that IscR is not involved in the regulation of nuclease colicins, but that the AsnC protein is. We report that AsnC, in concert with LexA, is the key controller of the temporal induction of the DNA degrading colicin E8 gene (cea8), after DNA damage. We demonstrate that a large AsnC nucleosome-like structure, in conjunction with two LexA molecules, prevent cea8 transcription initiation and that AsnC binding activity is directly modulated by L asparagine. We show that L-asparagine is an environmental factor that has a marked impact on cea8 promoter regulation. Our results show that AsnC also modulates the expression of several other DNase and RNase colicin genes but does not substantially affect pore-forming colicin K gene expression. We propose that selection pressure has "chosen" highly conserved regulators to control colicin expression in E. coli strains, enabling similar colicin gene silencing among bacteria upon exchange of colicinogenic plasmids.

KW - DNA damage

KW - Promoter regions

KW - DNA-binding proteins

KW - Nucleases

KW - Regulator genes

KW - Deoxyribonucleases

KW - Electrophoretic mobility shift assay

KW - Gene expression

U2 - 10.1371/journal.pgen.1005354

DO - 10.1371/journal.pgen.1005354

M3 - Article

C2 - 26114960

VL - 11

JO - PLoS Genetics

JF - PLoS Genetics

SN - 1553-7390

IS - 6

M1 - e1005354

ER -