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A Rad51 presynaptic filament is sufficient to capture nucleosomal homology during recombinational repair of a DNA double-strand break.


ABSTRACT: Repair of chromosomal DNA double-strand breaks by homologous recombination is essential for cell survival and genome stability. Within eukaryotic cells, this repair pathway requires a search for a homologous donor sequence and a subsequent strand invasion event on chromatin fibers. We employ a biotin-streptavidin minichromosome capture assay to show that yRad51 or hRad51 presynaptic filaments are sufficient to locate a homologous sequence and form initial joints, even on the surface of a nucleosome. Furthermore, we present evidence that the Rad54 chromatin-remodeling enzyme functions to convert these initial metastable products of the homology search to a stable joint molecule that is competent for subsequent steps of the repair process. Thus, contrary to popular belief, nucleosomes do not pose a potent barrier for successful recognition and capture of homology by an invading presynaptic filament.

SUBMITTER: Sinha M 

PROVIDER: S-EPMC4461863 | biostudies-literature | 2008 Jun

REPOSITORIES: biostudies-literature

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A Rad51 presynaptic filament is sufficient to capture nucleosomal homology during recombinational repair of a DNA double-strand break.

Sinha Manisha M   Peterson Craig L CL  

Molecular cell 20080601 6


Repair of chromosomal DNA double-strand breaks by homologous recombination is essential for cell survival and genome stability. Within eukaryotic cells, this repair pathway requires a search for a homologous donor sequence and a subsequent strand invasion event on chromatin fibers. We employ a biotin-streptavidin minichromosome capture assay to show that yRad51 or hRad51 presynaptic filaments are sufficient to locate a homologous sequence and form initial joints, even on the surface of a nucleos  ...[more]

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