Recruitment of Rad51 and Rad52 to Short Telomeres Triggers a Mec1-Mediated Hypersensitivity to Double-Stranded DNA Breaks in Senescent Budding Yeast

摘要: Telomere maintenance is required for chromosome stability, and telomeres are typically replicated by the action of telomerase. In both mammalian tumor yeast cells that lack telomerase, maintained an alternative recombination mechanism. Here we demonstrated budding Saccharomyces cerevisiae type I survivors derived from telomerase-deficient were hypersensitive to DNA damaging agents. Assays track telomere lengths drug sensitivity spore colonies suggested a correlation between shortening bleomycin sensitivity. Our genetic studies this depends on Mec1, which signals checkpoint activation, leading prolonged cell-cycle arrest in senescent yeasts. Moreover, also observed when equipped with short telomeres, recruitments homologous proteins, Rad51 Rad52, reduced at HO-endonuclease-catalyzed double-strand break (DSB), while their associations increased ends. These results sensitive phenotype may be attributed sequestration repair proteins compromised thus limiting capacity bona fide DSB sites.