ArticleMolecular microbiology2009
DnaAcos hyperinitiates by circumventing regulatory pathways that control the frequency of initiation in Escherichia coli.
Article in Molecular microbiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Review
- The plasmid-borne quinolone resistance protein QnrB, a novel DnaA-binding protein, increases the bacterial mutation rate by triggering DNA replication stress.Molecular microbiology · 2019Article
- Countermeasures to survive excessive chromosome replication in Escherichia coli.Current genetics · 2018Review
- Targeting the Bacterial Orisome in the Search for New Antibiotics.Frontiers in microbiology · 2017Article
- Mutant DnaAs of Escherichia coli that are refractory to negative control.Nucleic acids research · 2013Article
- Chromosome Replication in Escherichia coli: Life on the Scales.Life (Basel, Switzerland) · 2012Article
- Evidence for roles of the Escherichia coli Hda protein beyond regulatory inactivation of DnaA.Molecular microbiology · 2012Article
- The rcbA gene product reduces spontaneous and induced chromosome breaks in Escherichia coli.Journal of bacteriology · 2012Article
- Regulation of chromosomal replication initiation by oriC-proximal DnaA-box clusters in Bacillus subtilis.Nucleic acids research · 2012Article
- DnaA protein DNA-binding domain binds to Hda protein to promote inter-AAA+ domain interaction involved in regulatory inactivation of DnaA.The Journal of biological chemistry · 2011Article
- Mutations in the Bacillus subtilis beta clamp that separate its roles in DNA replication from mismatch repair.Journal of bacteriology · 2010Article
- Regulation of the replication cycle: conserved and diverse regulatory systems for DnaA and oriC.Nature reviews. Microbiology · 2010Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Mutants of dnaAcos are inviable at 30 degrees C because DnaAcos hyperinitiates, leading to new replication forks that apparently collide from behind with stalled forks, thereby generating lethal double-strand breaks. By comparison, an elevated level of DnaA also induces extra initiations, but lethality occurs only in strains defective in repairing double-strand breaks. To explore the model that the chromosomal level of DnaAcos, or the increased abundance of DnaA, increases initiation frequency by, escaping or overcoming pathways that control initiation, respectively, we developed a genetic selection and identified seqA, datA, dnaN and hda, which function in pathways that either act at oriC or modulate DnaA activity. To assess each pathway's relative effectiveness, we used genetically inactivated strains, and quantified initiation frequency after elevating the level of DnaA. The results indicate that the hda-dependent pathway has a stronger effect on initiation than pathways involving seqA and datA. Testing the model that DnaAcos overinitiates because it fails to respond to one or more regulatory mechanisms, we show that dnaAcos is unresponsive to hda and dnaN, which encodes the beta clamp, and also datA, a locus proposed to titer excess DnaA. These results explain how DnaAcos hyperinitiates to interfere with viability.
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