A Rad51 presynaptic filament is sufficient to capture nucleosomal homology during recombinational repair of a DNA double-strand break
Graduate School of Biomedical Sciences; Program in Molecular Medicine
Life Sciences | Medicine and Health Sciences
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.
DOI of Published Version
Mol Cell. 2008 Jun 20;30(6):803-10. Link to article on publisher's site
Sinha M, Peterson CL. (2008). A Rad51 presynaptic filament is sufficient to capture nucleosomal homology during recombinational repair of a DNA double-strand break. GSBS Student Publications. https://doi.org/10.1016/j.molcel.2008.04.015. Retrieved from https://escholarship.umassmed.edu/gsbs_sp/1361