Transcriptional coupling of DNA repair in sporulating B acillus subtilis cells

Summary In conditions of halted or limited genome replication, like those experienced in sporulating cells of B acillus subtilis, a more immediate detriment caused by DNA damage is altering the transcriptional programme that drives this developmental process. Here, we report that mfd , which encodes...

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Published inMolecular microbiology Vol. 90; no. 5; pp. 1088 - 1099
Main Authors Ramírez‐Guadiana, Fernando H., del Carmen Barajas‐Ornelas, Rocío, Ayala‐García, Víctor M., Yasbin, Ronald E., Robleto, Eduardo, Pedraza‐Reyes, Mario
Format Journal Article
LanguageEnglish
Published 01.12.2013
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Summary:Summary In conditions of halted or limited genome replication, like those experienced in sporulating cells of B acillus subtilis, a more immediate detriment caused by DNA damage is altering the transcriptional programme that drives this developmental process. Here, we report that mfd , which encodes a conserved bacterial protein that mediates transcription‐coupled DNA repair ( TCR ), is expressed together with uvrA in both compartments of B . subtilis sporangia. The function of Mfd was found to be important for processing the genetic damage during B . subtilis sporulation. Disruption of mfd sensitized developing spores to mitomycin‐ C ( M ‐ C ) treatment and UV ‐ C irradiation. Interestingly, in non‐growing sporulating cells, Mfd played an anti‐mutagenic role as its absence promoted UV ‐induced mutagenesis through a pathway involving YqjH / YqjW ‐mediated translesion synthesis ( TLS ). Two observations supported the participation of Mfd ‐dependent TCR in spore morphogenesis: (i) disruption of mfd notoriously affected the efficiency of B . subtilis sporulation and (ii) in comparison with the wild‐type strain, a significant proportion of Mfd ‐deficient sporangia that survived UV ‐ C treatment developed an asporogenous phenotype. We propose that the Mfd ‐dependent repair pathway operates during B . subtilis sporulation and that its function is required to eliminate genetic damage from transcriptionally active genes.
ISSN:0950-382X
1365-2958
DOI:10.1111/mmi.12417