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DnaA and LexA Proteins Regulate Transcription of the uvrB Gene in Escherichia coli: The Role of DnaA in the Control of the SOS Regulon

The uvrB gene belongs to the SOS network, encoding a key component of the nucleotide excision repair. The uvrB promoter region contains three identified promoters with four LexA binding sites, one consensus and six potential DnaA binding sites. A more than threefold increase in transcription of the...

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Autores principales: Wurihan, Gezi, Brambilla, Elisa, Wang, Shuwen, Sun, Hongwei, Fan, Lifei, Shi, Yixin, Sclavi, Bianca, Morigen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6015884/
https://www.ncbi.nlm.nih.gov/pubmed/29967594
http://dx.doi.org/10.3389/fmicb.2018.01212
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author Wurihan,
Gezi,
Brambilla, Elisa
Wang, Shuwen
Sun, Hongwei
Fan, Lifei
Shi, Yixin
Sclavi, Bianca
Morigen,
author_facet Wurihan,
Gezi,
Brambilla, Elisa
Wang, Shuwen
Sun, Hongwei
Fan, Lifei
Shi, Yixin
Sclavi, Bianca
Morigen,
author_sort Wurihan,
collection PubMed
description The uvrB gene belongs to the SOS network, encoding a key component of the nucleotide excision repair. The uvrB promoter region contains three identified promoters with four LexA binding sites, one consensus and six potential DnaA binding sites. A more than threefold increase in transcription of the chromosomal uvrB gene is observed in both the ΔlexA ΔsulA cells and dnaA(A345S) cells, and a fivefold increase in the ΔlexA ΔsulA dnaA(A345S) cells relative to the wild-type cells. The full activity of the uvrB promoter region requires both the uvrBp1-2 and uvrBp3 promoters and is repressed by both the DnaA and LexA proteins. LexA binds tightly to LexA-box1 at the uvrBp1-2 promoter irrespective of the presence of DnaA and this binding is important for the control of the uvrBp1-2 promoter. DnaA and LexA, however, compete for binding to and regulation of the uvrBp3 promoter in which the DnaA-box6 overlaps with LexA-box4. The transcription control of uvrBp3 largely depends on DnaA-box6. Transcription of other SOS regulon genes, such as recN and dinJ, is also repressed by both DnaA and LexA. Interestingly, the absence of LexA in the presence of the DnaA(A345S) mutant leads to production of elongated cells with incomplete replication, aberrant nucleoids and slow growth. We propose that DnaA is a modulator for maintenance of genome integrity during the SOS response by limiting the expression of the SOS regulon.
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spelling pubmed-60158842018-07-02 DnaA and LexA Proteins Regulate Transcription of the uvrB Gene in Escherichia coli: The Role of DnaA in the Control of the SOS Regulon Wurihan, Gezi, Brambilla, Elisa Wang, Shuwen Sun, Hongwei Fan, Lifei Shi, Yixin Sclavi, Bianca Morigen, Front Microbiol Microbiology The uvrB gene belongs to the SOS network, encoding a key component of the nucleotide excision repair. The uvrB promoter region contains three identified promoters with four LexA binding sites, one consensus and six potential DnaA binding sites. A more than threefold increase in transcription of the chromosomal uvrB gene is observed in both the ΔlexA ΔsulA cells and dnaA(A345S) cells, and a fivefold increase in the ΔlexA ΔsulA dnaA(A345S) cells relative to the wild-type cells. The full activity of the uvrB promoter region requires both the uvrBp1-2 and uvrBp3 promoters and is repressed by both the DnaA and LexA proteins. LexA binds tightly to LexA-box1 at the uvrBp1-2 promoter irrespective of the presence of DnaA and this binding is important for the control of the uvrBp1-2 promoter. DnaA and LexA, however, compete for binding to and regulation of the uvrBp3 promoter in which the DnaA-box6 overlaps with LexA-box4. The transcription control of uvrBp3 largely depends on DnaA-box6. Transcription of other SOS regulon genes, such as recN and dinJ, is also repressed by both DnaA and LexA. Interestingly, the absence of LexA in the presence of the DnaA(A345S) mutant leads to production of elongated cells with incomplete replication, aberrant nucleoids and slow growth. We propose that DnaA is a modulator for maintenance of genome integrity during the SOS response by limiting the expression of the SOS regulon. Frontiers Media S.A. 2018-06-18 /pmc/articles/PMC6015884/ /pubmed/29967594 http://dx.doi.org/10.3389/fmicb.2018.01212 Text en Copyright © 2018 Wurihan, Gezi, Brambilla, Wang, Sun, Fan, Shi, Sclavi and Morigen. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Microbiology
Wurihan,
Gezi,
Brambilla, Elisa
Wang, Shuwen
Sun, Hongwei
Fan, Lifei
Shi, Yixin
Sclavi, Bianca
Morigen,
DnaA and LexA Proteins Regulate Transcription of the uvrB Gene in Escherichia coli: The Role of DnaA in the Control of the SOS Regulon
title DnaA and LexA Proteins Regulate Transcription of the uvrB Gene in Escherichia coli: The Role of DnaA in the Control of the SOS Regulon
title_full DnaA and LexA Proteins Regulate Transcription of the uvrB Gene in Escherichia coli: The Role of DnaA in the Control of the SOS Regulon
title_fullStr DnaA and LexA Proteins Regulate Transcription of the uvrB Gene in Escherichia coli: The Role of DnaA in the Control of the SOS Regulon
title_full_unstemmed DnaA and LexA Proteins Regulate Transcription of the uvrB Gene in Escherichia coli: The Role of DnaA in the Control of the SOS Regulon
title_short DnaA and LexA Proteins Regulate Transcription of the uvrB Gene in Escherichia coli: The Role of DnaA in the Control of the SOS Regulon
title_sort dnaa and lexa proteins regulate transcription of the uvrb gene in escherichia coli: the role of dnaa in the control of the sos regulon
topic Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6015884/
https://www.ncbi.nlm.nih.gov/pubmed/29967594
http://dx.doi.org/10.3389/fmicb.2018.01212
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