ArticleGenes & development2011
A DNA damage checkpoint in Caulobacter crescentus inhibits cell division through a direct interaction with FtsW.
Article in Genes & development, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 82 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
82 citing papers in PubMed, 140 citations in OpenAlex.
- An ancestral transmembrane transcription factor couples cell envelope regulation and the SOS response in Caulobacter crescentus.PLoS genetics · 2026Article
- Cytosine methylation contributes to the fitness ofiScience · 2026Article
- Variability in intrinsic promoter strength underlies the temporal hierarchy of the Caulobacter SOS response induction.PLoS biology · 2025Article
- PIRT-Seq: a high-resolution whole-genome assay to identify protein-coding genes.Nucleic acids research · 2025Article
- Transient inhibition of cell division in competent pneumococcal cells results from deceleration of the septal peptidoglycan complex.Nature communications · 2025Article
- Live tracking of replisomes reveals nutrient-dependent regulation of replication elongation rates in Caulobacter crescentus.Current biology : CB · 2025Article
- Large Roles of Small Proteins.Annual review of microbiology · 2024Review
- The divisome is a self-enhancing machine in Escherichia coli and Caulobacter crescentus.Nature communications · 2024Article
- GTPase activity regulates FtsZ ring positioning inMolecular biology of the cell · 2024Article
- Cell cycle dependent coordination of surface layer biogenesis in Caulobacter crescentus.Nature communications · 2024Article
- Widespread prevalence of a methylation-dependent switch to activate an essential DNA damage response in bacteria.PLoS biology · 2024Article
- The global RNA-RNA interactome ofProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Integration of cell wall synthesis and chromosome segregation during cell division in Caulobacter.The Journal of cell biology · 2024Article
- Proteomic survey of the DNA damage response inJournal of bacteriology · 2023Article
- Proteomic survey of the DNA damage response inbioRxiv : the preprint server for biology · 2023Article
- Allosteric activation of cell wall synthesis during bacterial growth.Nature communications · 2023Article
- SOS-independent bacterial DNA damage responses: diverse mechanisms, unifying function.Current opinion in microbiology · 2023Review
- Cell division protein FtsK coordinates bacterial chromosome segregation and daughter cell separation in Staphylococcus aureus.The EMBO journal · 2023Article
- FtsZ phosphorylation brings about growth arrest upon DNA damage inFASEB bioAdvances · 2023Article
- Mechanistic insight into the repair of C8-linked pyrrolobenzodiazepine monomer-mediated DNA damage.RSC medicinal chemistry · 2022Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
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.
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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.