A DNA Damage-Induced, SOS-Independent Checkpoint Regulates Cell Division in Caulobacter crescentus
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Modell-2014-A DNA Damage-Induced.pdf
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8.6 MB
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Author(s)
Modell, Joshua W.
Kambara, Tracy K.
Perchuk, Barrett
Laub, Michael T
Date Issued
October 2014
Journal
PLoS Biology
Publisher
Public Library of Science
Citation
Modell, Joshua W., Tracy K. Kambara, Barrett S. Perchuk, and Michael T. Laub. “A DNA Damage-Induced, SOS-Independent Checkpoint Regulates Cell Division in Caulobacter Crescentus.” Edited by Bénédicte Michel. PLoS Biology 12, no. 10 (October 28, 2014): e1001977.
Version
Final published version
Abstract
Cells must coordinate DNA replication with cell division, especially during episodes of DNA damage. The paradigm for cell division control following DNA damage in bacteria involves the SOS response where cleavage of the transcriptional repressor LexA induces a division inhibitor. However, in Caulobacter crescentus, cells lacking the primary SOS-regulated inhibitor, sidA, can often still delay division post-damage. Here we identify didA, a second cell division inhibitor that is induced by DNA damage, but in an SOS-independent manner. Together, DidA and SidA inhibit division, such that cells lacking both inhibitors divide prematurely following DNA damage, with lethal consequences. We show that DidA does not disrupt assembly of the division machinery and instead binds the essential division protein FtsN to block cytokinesis. Intriguingly, mutations in FtsW and FtsI, which drive the synthesis of septal cell wall material, can suppress the activity of both SidA and DidA, likely by causing the FtsW/I/N complex to hyperactively initiate cell division. Finally, we identify a transcription factor, DriD, that drives the SOS-independent transcription of didA following DNA damage.
MIT Department
Massachusetts Institute of Technology. Department of Biology
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Creative Commons Attribution
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DOI of Published Version
https://doi.org/10.1371/journal.pbio.1001977
