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The WalRK ( YycFG ) and σ I RsgI regulators cooperate to control CwlO and LytE expression in exponentially growing and stressed B acillus subtilis cells
The WalRK ( YycFG ) two‐component system co‐ordinates cell wall metabolism with growth by regulating expression of autolysins and proteins that modulate autolysin activity. Here we extend its role in cell wall metabolism by showing that WalR binds to 22 chromosomal loci in vivo . Among the newly ide...
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Published in: | Molecular microbiology 2013-01, Vol.87 (1), p.180-195 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | The
WalRK
(
YycFG
) two‐component system co‐ordinates cell wall metabolism with growth by regulating expression of autolysins and proteins that modulate autolysin activity. Here we extend its role in cell wall metabolism by showing that
WalR
binds to 22 chromosomal loci
in vivo
. Among the newly identified genes of the
WalRK
bindome are those that encode the wall‐associated protein
WapA
, the penicillin binding proteins
PbpH
and
Pbp
5, the minor teichoic acid synthetic enzymes
GgaAB
and the regulators σ
I
RsgI
. The putative
WalR
binding sequence at many newly identified binding loci deviates from the previously defined consensus. Moreover, expression of many newly identified operons is controlled by multiple regulators. An unusual feature is that
WalR
binds to an extended
DNA
region spanning multiple open reading frames at some loci.
WalRK
directly activates expression of the
sigIrsgI
operon from a newly identified σ
A
promoter and represses expression from the previously identified σ
I
promoter. We propose that this regulatory link between
WalRK
and σ
I
RsgI
expression ensures that the endopeptidase requirement (
CwlO
or
LytE
) for cell viability is fulfilled during growth and under stress conditions. Thus the
WalRK
and σ
I
RsgI
regulatory systems cooperate to control cell wall metabolism in growing and stressed cells. |
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ISSN: | 0950-382X 1365-2958 |
DOI: | 10.1111/mmi.12092 |