Characterization of RAD51-Independent Break-Induced Replication That Acts Preferentially with Short Homologous Sequences
AUTOR(ES)
Ira, Grzegorz
FONTE
American Society for Microbiology
RESUMO
Repair of double-strand breaks by gene conversions between homologous sequences located on different Saccharomyces cerevisiae chromosomes or plasmids requires RAD51. When repair occurs between inverted repeats of the same plasmid, both RAD51-dependent and RAD51-independent repairs are found. Completion of RAD51-independent plasmid repair events requires RAD52, RAD50, RAD59, TID1 (RDH54), and SRS2 and appears to involve break-induced replication coupled to single-strand annealing. Surprisingly, RAD51-independent recombination requires much less homology (30 bp) for strand invasion than does RAD51-dependent repair (approximately 100 bp); in fact, the presence of Rad51p impairs recombination with short homology. The differences between the RAD51- and RAD50/RAD59-dependent pathways account for the distinct ways that two different recombination processes maintain yeast telomeres in the absence of telomerase.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=135638Documentos Relacionados
- RAD51-independent break-induced replication to repair a broken chromosome depends on a distant enhancer site
- RAD51-Dependent Break-Induced Replication in Yeast
- Genetic Requirements for RAD51- and RAD54-Independent Break-Induced Replication Repair of a Chromosomal Double-Strand Break
- RAD51-Dependent Break-Induced Replication Differs in Kinetics and Checkpoint Responses from RAD51-Mediated Gene Conversion
- Overexpression of human RAD51 and RAD52 reduces double-strand break-induced homologous recombination in mammalian cells