Abstract：
:The yeast Sir2/3/4p complex is found in abundance at telomeres, where it participates in the formation of silent heterochromatin and telomere maintenance. Here, we show that Sir3p is released from telomeres in response to DNA double-strand breaks (DSBs), binds to DSBs, and mediates their repair, independent of cell mating type. Sir3p relocalization is S phase specific and, importantly, requires the DNA damage checkpoint genes MEC1 and RAD9. MEC1 is a homolog of ATM, mutations in which cause ataxia telangiectasia (A-T), a disease characterized by various neurologic and immunologic abnormalities, a predisposition for cancer, and a cellular defect in repair of DSBs. This novel mode by which preformed DNA repair machinery is mobilized by DNA damage sensors may have implications for human diseases resulting from defective DSB repair.
journal_name
Celljournal_title
Cellauthors
Mills KD,Sinclair DA,Guarente Ldoi
10.1016/s0092-8674(00)80772-2subject
Has Abstractpub_date
1999-05-28 00:00:00pages
609-20issue
5eissn
0092-8674issn
1097-4172pii
S0092-8674(00)80772-2journal_volume
97pub_type
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