Journal
MOLECULAR CELL
Volume 30, Issue 1, Pages 73-85Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2008.01.016
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Funding
- NIGMS NIH HHS [T32 GM007088-33, GM67055, GM50237, R01 GM050237, F32 GM070088, GM70088, R01 GM067055, R01 GM050237-12, R01 GM067055-06, T32 GM007088, GM73568, F31 GM073568, F31 GM073568-03, R37 GM050237] Funding Source: Medline
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Double-strand breaks (DSBs) are potentially lethal DNA lesions that can be repaired by either homologous recombination (HR) or nonhomologous end-joining (NHEJ). We show that DSBs induced by ionizing radiation (IR) are efficiently processed for HR and bound by Rfa1 during G1, while endonuclease-induced breaks are recognized by Rfa1 only after the cell enters S phase. This difference is dependent on the DNA end-binding Yku70/Yku80 complex. Cell-cycle regulation is also observed in the DNA damage checkpoint response. Specifically, the 9-1-1 complex is required in G1 cells to recruit the Ddc2 checkpoint protein to damaged DNA, while, upon entry into S phase, the cyclin-dependent kinase Cdc28 and the 9-1-1 complex both serve to recruit Ddc2 to foci. Together, these results demonstrate that the DNA repair machinery distinguishes between different types of damage in G1, which translates into different modes of checkpoint activation in G1 and S/G2 cells.
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