Journal article
Rad54 dissociates homologous recombination intermediates by branch migration
Nature structural & molecular biology, Vol.14(8), pp.746-753
Aug 2007
PMID: 17660833
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
Double-strand DNA breaks (DSBs) cause cell death and genome instability. Homologous recombination is a major DSB repair pathway that operates by forming joint molecules with homologous DNA sequences, which are used as templates to achieve accurate repair. In eukaryotes, Rad51 protein (RecA homolog) searches for homologous sequences and catalyzes the formation of joint molecules (D-loops). Once joint molecules have been formed, DNA polymerase extends the 3' single-stranded DNA tails of the broken chromosome, restoring the lost information. How joint molecules subsequently dissociate is unknown. We reconstituted DSB repair in vitro using purified human homologous recombination proteins and DNA polymerase eta. We found that Rad54 protein, owing to its ATP-dependent branch-migration activity, can cause dissociation of joint molecules. These results suggest a previously uncharacterized mechanism of DSB repair in which Rad54 branch-migration activity plays an important role.
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Details
- Title
- Rad54 dissociates homologous recombination intermediates by branch migration
- Creators
- Dmitry V Bugreev - Department of Biochemistry and Molecular Biology, Drexel University College of Medicine, Philadelphia, Pennsylvania 19102-1192, USAFumio HanaokaAlexander V Mazin
- Publication Details
- Nature structural & molecular biology, Vol.14(8), pp.746-753
- Publisher
- Springer Nature; United States
- Grant note
- CA100839 / NCI NIH HHS
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Biochemistry and Molecular Biology
- Identifiers
- 991014878356504721
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- Domestic collaboration
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- Web of Science research areas
- Biochemistry & Molecular Biology
- Biophysics
- Cell Biology