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Genes Dev. 2011 Jun 15;25(12):1328-43. doi: 10.1101/gad.2038911.

A DNA damage checkpoint in Caulobacter crescentus inhibits cell division through a direct interaction with FtsW.

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1
Department of Biology, Massachusetts Institute of Technology, Cambridge, USA.

Erratum in

  • Genes Dev. 2011 Aug 1;25(15):1662.

Abstract

Following DNA damage, cells typically delay cell cycle progression and inhibit cell division until their chromosomes have been repaired. The bacterial checkpoint systems responsible for these DNA damage responses are incompletely understood. Here, we show that Caulobacter crescentus responds to DNA damage by coordinately inducing an SOS regulon and inhibiting the master regulator CtrA. Included in the SOS regulon is sidA (SOS-induced inhibitor of cell division A), a membrane protein of only 29 amino acids that helps to delay cell division following DNA damage, but is dispensable in undamaged cells. SidA is sufficient, when overproduced, to block cell division. However, unlike many other regulators of bacterial cell division, SidA does not directly disrupt the assembly or stability of the cytokinetic ring protein FtsZ, nor does it affect the recruitment of other components of the cell division machinery. Instead, we provide evidence that SidA inhibits division by binding directly to FtsW to prevent the final constriction of the cytokinetic ring.

PMID:
21685367
PMCID:
PMC3127433
DOI:
10.1101/gad.2038911
[Indexed for MEDLINE]
Free PMC Article
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