AUTHOR=Moreno-del Alamo María , Torres Rubén , Manfredi Candela , Ruiz-Masó José A. , del Solar Gloria , Alonso Juan Carlos 

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

JOURNAL=Frontiers in Molecular Biosciences

VOLUME=7

YEAR=2020

URL=https://www.frontiersin.org/journals/molecular-biosciences/articles/10.3389/fmolb.2020.00140

DOI=10.3389/fmolb.2020.00140

ISSN=2296-889X

ABSTRACT=<p><italic>Bacillus subtilis</italic> PcrA abrogates replication-transcription conflicts <italic>in vivo</italic> and disrupts RecA nucleoprotein filaments <italic>in vitro</italic>. Inactivation of <italic>pcrA</italic> is lethal. We show that PcrA depletion lethality is suppressed by <italic>recJ</italic> (involved in end resection), <italic>recA</italic> (the recombinase), or <italic>mfd</italic> (transcription-coupled repair) inactivation, but not by inactivating end resection (<italic>addAB</italic> or <italic>recQ</italic>), positive and negative RecA modulators (<italic>rarA</italic> or <italic>recX</italic> and <italic>recU</italic>), or genes involved in the reactivation of a stalled RNA polymerase (<italic>recD</italic>2, <italic>helD, hepA</italic>, and <italic>ywqA</italic>). We also report that <italic>B. subtilis</italic> mutations previously designated as <italic>recL16</italic> actually map to the <italic>recO</italic> locus, and confirm that PcrA depletion lethality is suppressed by <italic>recO</italic> inactivation. The <italic>pcrA</italic> gene is epistatic to <italic>recA</italic> or <italic>mfd</italic>, but it is not epistatic to <italic>addAB, recJ, recQ, recO16, rarA, recX, recU, recD</italic>2, <italic>helD, hepA</italic>, or <italic>ywqA</italic> in response to DNA damage. PcrA depletion led to the accumulation of unsegregated chromosomes, and this defect is increased by <italic>recQ, rarA</italic>, or <italic>recU</italic> inactivation. We propose that PcrA, which is crucial to maintain cell viability, is involved in different DNA transactions.</p>