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 in | Molecular microbiology Vol. 90; no. 5; pp. 1088 - 1099 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
01.12.2013
|
Online Access | Get full text |
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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. |
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ISSN: | 0950-382X 1365-2958 |
DOI: | 10.1111/mmi.12417 |