ArticlePLoS genetics2017
Global analysis of double-strand break processing reveals in vivo properties of the helicase-nuclease complex AddAB.
Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Chromosome topology gates productive RecA homology search.bioRxiv : the preprint server for biology · 2026Article
- SSB-mediated enhancement of argonaute activity triggers SOS filamentation in bacteria.Nucleic acids research · 2026Article
- 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
- SMC protein RecN drives RecA filament translocation for in vivo homology search.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Essential Role for an Isoform of Escherichia coli Translation Initiation Factor IF2 in Repair of Two-Ended DNA Double-Strand Breaks.Journal of bacteriology · 2022Article
- Optimized two-step electroporation process to achieve efficient nonviral-mediated gene insertion into primary T cells.FEBS open bio · 2022Article
- Asymmetric chromosome segregation and cell division in DNA damage-induced bacterial filaments.Molecular biology of the cell · 2020Article
- The RecB helicase-nuclease tether mediates Chi hotspot control of RecBCD enzyme.Nucleic acids research · 2019Article
- Direct observation of end resection by RecBCD during double-stranded DNA break repair in vivo.Nucleic acids research · 2018Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
Abstract
In bacteria, double-strand break (DSB) repair via homologous recombination is thought to be initiated through the bi-directional degradation and resection of DNA ends by a helicase-nuclease complex such as AddAB. The activity of AddAB has been well-studied in vitro, with translocation speeds between 400-2000 bp/s on linear DNA suggesting that a large section of DNA around a break site is processed for repair. However, the translocation rate and activity of AddAB in vivo is not known, and how AddAB is regulated to prevent excessive DNA degradation around a break site is unclear. To examine the functions and mechanistic regulation of AddAB inside bacterial cells, we developed a next-generation sequencing-based approach to assay DNA processing after a site-specific DSB was introduced on the chromosome of Caulobacter crescentus. Using this assay we determined the in vivo rates of DSB processing by AddAB and found that putative chi sites attenuate processing in a RecA-dependent manner. This RecA-mediated regulation of AddAB prevents the excessive loss of DNA around a break site, limiting the effects of DSB processing on transcription. In sum, our results, taken together with prior studies, support a mechanism for regulating AddAB that couples two key events of DSB repair-the attenuation of DNA-end processing and the initiation of homology search by RecA-thereby helping to ensure that genomic integrity is maintained during DSB repair.
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