ArticlePLoS biology2014
A DNA damage-induced, SOS-independent checkpoint regulates cell division in Caulobacter crescentus.
Article in PLoS biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
80 citing papers in PubMed, 58 citations in OpenAlex.
- A LexA-independent redox-based transcriptional regulation to DNA damage response system in mycobacteria.BMC microbiology · 2026Article
- Control of cell division by anbioRxiv : the preprint server for biology · 2026Article
- Peptidoglycan recycling is critical for cell division, cell wall integrity, and β-lactam resistance ineLife · 2026Article
- Transcription activation mechanism of a noncanonical DNA damage response pathway by the WYL-activator, DriD.Science advances · 2026Article
- A WYL transcriptional regulator activates the DNA damage response pathway in Acinetobacter species.Nucleic acids research · 2026Article
- Stress testing reveals selective vulnerabilities in protein homeostasis.Cell reports · 2026Article
- Cytosine methylation contributes to the fitness ofiScience · 2026Article
- Mechanistic Insights into the Antimicrobial Effect of Benzodioxane-Benzamides AgainstAntibiotics (Basel, Switzerland) · 2026Article
- DdiA, an XRE family transcriptional regulator, is a co-regulator of the DNA damage response inJournal of bacteriology · 2025Article
- The hit-and-run of cell wall synthesis: LpoB transiently binds and activates PBP1b through a conserved allosteric switch.Nature communications · 2025Article
- Transient inhibition of cell division in competent pneumococcal cells results from deceleration of the septal peptidoglycan complex.Nature communications · 2025Article
- Allosteric activation mechanism of DriD, a WYL-domain containing transcription regulator.Communications biology · 2025Article
- Single-stranded DNA binding to the transcription factor PafBC triggers the mycobacterial DNA damage response.Science advances · 2025Article
- The cell division protein FzlA performs a conserved function in diverse alphaproteobacteria.Journal of bacteriology · 2024Article
- The divisome is a self-enhancing machine in Escherichia coli and Caulobacter crescentus.Nature communications · 2024Article
- Cell cycle dependent coordination of surface layer biogenesis in Caulobacter crescentus.Nature communications · 2024Article
- Article
- Widespread prevalence of a methylation-dependent switch to activate an essential DNA damage response in bacteria.PLoS biology · 2024Article
- Structure of the WYL-domain containing transcription activator, DriD, in complex with ssDNA effector and DNA target site.Nucleic acids research · 2024Article
- Integration of cell wall synthesis and chromosome segregation during cell division in Caulobacter.The Journal of cell biology · 2024Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.