ArticleNucleic acids research2016
Chi hotspots trigger a conformational change in the helicase-like domain of AddAB to activate homologous recombination.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- OT-Curtains: an approach for studying protein interactions with DNA ends using optical tweezers and confocal fluorescence microscopy.Nucleic acids research · 2026Article
- Insight into the biochemical mechanism of DNA helicases provided by bulk-phase and single-molecule assays.Methods (San Diego, Calif.) · 2022Review
- Modeling DNA Unwinding by AddAB Helicase-Nuclease and Modulation by Chi Sequences: Comparison with AdnAB and RecBCD.Cellular and molecular bioengineering · 2019Article
- Global analysis of double-strand break processing reveals in vivo properties of the helicase-nuclease complex AddAB.PLoS genetics · 2017Article
- Homologous recombination mediated by the mycobacterial AdnAB helicase without end resection by the AdnAB nucleases.Nucleic acids research · 2017Article
- Mechanism for nuclease regulation in RecBCD.eLife · 2016Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
In bacteria, the repair of double-stranded DNA breaks is modulated by Chi sequences. These are recognised by helicase-nuclease complexes that process DNA ends for homologous recombination. Chi activates recombination by changing the biochemical properties of the helicase-nuclease, transforming it from a destructive exonuclease into a recombination-promoting repair enzyme. This transition is thought to be controlled by the Chi-dependent opening of a molecular latch, which enables part of the DNA substrate to evade degradation beyond Chi. Here, we show that disruption of the latch improves Chi recognition efficiency and stabilizes the interaction of AddAB with Chi, even in mutants that are impaired for Chi binding. Chi recognition elicits a structural change in AddAB that maps to a region of AddB which resembles a helicase domain, and which harbours both the Chi recognition locus and the latch. Mutation of the latch potentiates the change and moderately reduces the duration of a translocation pause at Chi. However, this mutant displays properties of Chi-modified AddAB even in the complete absence of bona fide hotspot sequences. The results are used to develop a model for AddAB regulation in which allosteric communication between Chi binding and latch opening ensures quality control during recombination hotspot recognition.
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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.