AI Article Synopsis
- The repair of double-stranded DNA breaks through homologous recombination relies on processing the broken ends to allow for DNA strand exchange.
- Human BLM helicase enhances the activity of exonuclease 1 (hExo1), specifically promoting the resection of DNA while not relying on the helicase activity of BLM itself.
- This process enables the resected DNA ends to interact with Rad51, facilitating homologous DNA pairing, which is crucial for effective DNA repair.
Article Abstract
The error-free repair of double-stranded DNA breaks by homologous recombination requires processing of broken ends. These processed ends are substrates for assembly of DNA strand exchange proteins that mediate DNA strand invasion. Here, we establish that human BLM helicase, a member of the RecQ family, stimulates the nucleolytic activity of human exonuclease 1 (hExo1), a 5'-->3' double-stranded DNA exonuclease. The stimulation is specific because other RecQ homologs fail to stimulate hExo1. Stimulation of DNA resection by hExo1 is independent of BLM helicase activity and is, instead, mediated by an interaction between the 2 proteins. Finally, we show that DNA ends resected by hExo1 and BLM are used by human Rad51, but not its yeast or bacterial counterparts, to promote homologous DNA pairing. This in vitro system recapitulates initial steps of homologous recombination and provides biochemical evidence for a role of BLM and Exo1 in the initiation of recombinational DNA repair.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2579351 | PMC |
| http://dx.doi.org/10.1073/pnas.0809380105 | DOI Listing |
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