Bacillus subtilis PcrA Couples DNA Replication, Transcription, Recombination and Segregation

Bacillus subtilis PcrA abrogates replication-transcription conflicts in vivo and disrupts RecA nucleoprotein filaments in vitro. Inactivation of pcrA is lethal. We show that PcrA depletion lethality is suppressed by recJ (involved in end resection), recA (the recombinase), or mfd (transcription-coup...

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Published inFrontiers in molecular biosciences Vol. 7; p. 140
Main Authors Moreno-del Alamo, María, Torres, Rubén, Manfredi, Candela, Ruiz-Masó, José A., del Solar, Gloria, Alonso, Juan Carlos
Format Journal Article
LanguageEnglish
Published Frontiers Media S.A 21.07.2020
Subjects
Molecular Biosciences
RecL16
Rep
replication fork stalling
replication-transcription conflict
RNA polymerase backtracking
UvrD
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Abstract Bacillus subtilis PcrA abrogates replication-transcription conflicts in vivo and disrupts RecA nucleoprotein filaments in vitro. Inactivation of pcrA is lethal. We show that PcrA depletion lethality is suppressed by recJ (involved in end resection), recA (the recombinase), or mfd (transcription-coupled repair) inactivation, but not by inactivating end resection (addAB or recQ), positive and negative RecA modulators (rarA or recX and recU), or genes involved in the reactivation of a stalled RNA polymerase (recD2, helD, hepA, and ywqA). We also report that B. subtilis mutations previously designated as recL16 actually map to the recO locus, and confirm that PcrA depletion lethality is suppressed by recO inactivation. The pcrA gene is epistatic to recA or mfd, but it is not epistatic to addAB, recJ, recQ, recO16, rarA, recX, recU, recD2, helD, hepA, or ywqA in response to DNA damage. PcrA depletion led to the accumulation of unsegregated chromosomes, and this defect is increased by recQ, rarA, or recU inactivation. We propose that PcrA, which is crucial to maintain cell viability, is involved in different DNA transactions.Bacillus subtilis PcrA abrogates replication-transcription conflicts in vivo and disrupts RecA nucleoprotein filaments in vitro. Inactivation of pcrA is lethal. We show that PcrA depletion lethality is suppressed by recJ (involved in end resection), recA (the recombinase), or mfd (transcription-coupled repair) inactivation, but not by inactivating end resection (addAB or recQ), positive and negative RecA modulators (rarA or recX and recU), or genes involved in the reactivation of a stalled RNA polymerase (recD2, helD, hepA, and ywqA). We also report that B. subtilis mutations previously designated as recL16 actually map to the recO locus, and confirm that PcrA depletion lethality is suppressed by recO inactivation. The pcrA gene is epistatic to recA or mfd, but it is not epistatic to addAB, recJ, recQ, recO16, rarA, recX, recU, recD2, helD, hepA, or ywqA in response to DNA damage. PcrA depletion led to the accumulation of unsegregated chromosomes, and this defect is increased by recQ, rarA, or recU inactivation. We propose that PcrA, which is crucial to maintain cell viability, is involved in different DNA transactions.
AbstractList Bacillus subtilis PcrA abrogates replication-transcription conflicts in vivo and disrupts RecA nucleoprotein filaments in vitro. Inactivation of pcrA is lethal. We show that PcrA depletion lethality is suppressed by recJ (involved in end resection), recA (the recombinase), or mfd (transcription-coupled repair) inactivation, but not by inactivating end resection (addAB or recQ), positive and negative RecA modulators (rarA or recX and recU), or genes involved in the reactivation of a stalled RNA polymerase (recD2, helD, hepA, and ywqA). We also report that B. subtilis mutations previously designated as recL16 actually map to the recO locus, and confirm that PcrA depletion lethality is suppressed by recO inactivation. The pcrA gene is epistatic to recA or mfd, but it is not epistatic to addAB, recJ, recQ, recO16, rarA, recX, recU, recD2, helD, hepA, or ywqA in response to DNA damage. PcrA depletion led to the accumulation of unsegregated chromosomes, and this defect is increased by recQ, rarA, or recU inactivation. We propose that PcrA, which is crucial to maintain cell viability, is involved in different DNA transactions.Bacillus subtilis PcrA abrogates replication-transcription conflicts in vivo and disrupts RecA nucleoprotein filaments in vitro. Inactivation of pcrA is lethal. We show that PcrA depletion lethality is suppressed by recJ (involved in end resection), recA (the recombinase), or mfd (transcription-coupled repair) inactivation, but not by inactivating end resection (addAB or recQ), positive and negative RecA modulators (rarA or recX and recU), or genes involved in the reactivation of a stalled RNA polymerase (recD2, helD, hepA, and ywqA). We also report that B. subtilis mutations previously designated as recL16 actually map to the recO locus, and confirm that PcrA depletion lethality is suppressed by recO inactivation. The pcrA gene is epistatic to recA or mfd, but it is not epistatic to addAB, recJ, recQ, recO16, rarA, recX, recU, recD2, helD, hepA, or ywqA in response to DNA damage. PcrA depletion led to the accumulation of unsegregated chromosomes, and this defect is increased by recQ, rarA, or recU inactivation. We propose that PcrA, which is crucial to maintain cell viability, is involved in different DNA transactions.
Bacillus subtilis PcrA abrogates replication-transcription conflicts in vivo and disrupts RecA nucleoprotein filaments in vitro . Inactivation of pcrA is lethal. We show that PcrA depletion lethality is suppressed by recJ (involved in end resection), recA (the recombinase), or mfd (transcription-coupled repair) inactivation, but not by inactivating end resection ( addAB or recQ ), positive and negative RecA modulators ( rarA or recX and recU ), or genes involved in the reactivation of a stalled RNA polymerase ( recD 2, helD, hepA , and ywqA ). We also report that B. subtilis mutations previously designated as recL16 actually map to the recO locus, and confirm that PcrA depletion lethality is suppressed by recO inactivation. The pcrA gene is epistatic to recA or mfd , but it is not epistatic to addAB, recJ, recQ, recO16, rarA, recX, recU, recD 2, helD, hepA , or ywqA in response to DNA damage. PcrA depletion led to the accumulation of unsegregated chromosomes, and this defect is increased by recQ, rarA , or recU inactivation. We propose that PcrA, which is crucial to maintain cell viability, is involved in different DNA transactions.
Bacillus subtilis PcrA abrogates replication-transcription conflicts in vivo and disrupts RecA nucleoprotein filaments in vitro. Inactivation of pcrA is lethal. We show that PcrA depletion lethality is suppressed by recJ (involved in end resection), recA (the recombinase), or mfd (transcription-coupled repair) inactivation, but not by inactivating end resection (addAB or recQ), positive and negative RecA modulators (rarA or recX and recU), or genes involved in the reactivation of a stalled RNA polymerase (recD2, helD, hepA, and ywqA). We also report that B. subtilis mutations previously designated as recL16 actually map to the recO locus, and confirm that PcrA depletion lethality is suppressed by recO inactivation. The pcrA gene is epistatic to recA or mfd, but it is not epistatic to addAB, recJ, recQ, recO16, rarA, recX, recU, recD2, helD, hepA, or ywqA in response to DNA damage. PcrA depletion led to the accumulation of unsegregated chromosomes, and this defect is increased by recQ, rarA, or recU inactivation. We propose that PcrA, which is crucial to maintain cell viability, is involved in different DNA transactions.
Author Torres, Rubén
Alonso, Juan Carlos
Manfredi, Candela
Moreno-del Alamo, María
del Solar, Gloria
Ruiz-Masó, José A.
AuthorAffiliation 1 Department of Microbial Biotechnology, Centro Nacional de Biotecnología, CNB-CSIC , Madrid , Spain
2 Centro de Investigaciones Biológicas Margarita Salas, CIB-CSIC , Madrid , Spain
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This article was submitted to Molecular Recognition, a section of the journal Frontiers in Molecular Biosciences
Edited by: Chew Chieng Yeo, Sultan Zainal Abidin University, Malaysia
Present address: Candela Manfredi, Dept of Pediatrics, Emory University School of Medicine, Atlanta, GA, United States
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Snippet Bacillus subtilis PcrA abrogates replication-transcription conflicts in vivo and disrupts RecA nucleoprotein filaments in vitro. Inactivation of pcrA is...
Bacillus subtilis PcrA abrogates replication-transcription conflicts in vivo and disrupts RecA nucleoprotein filaments in vitro . Inactivation of pcrA is...
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StartPage 140
SubjectTerms Molecular Biosciences
RecL16
Rep
replication fork stalling
replication-transcription conflict
RNA polymerase backtracking
UvrD
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Title Bacillus subtilis PcrA Couples DNA Replication, Transcription, Recombination and Segregation
URI https://www.proquest.com/docview/2434477936
https://pubmed.ncbi.nlm.nih.gov/PMC7385302
https://doaj.org/article/38c8eefaa2024ae5936baa4852cb3216
Volume 7
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