期刊
JOURNAL OF CELL BIOLOGY
卷 170, 期 3, 页码 341-347出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200411083
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资金
- NCI NIH HHS [CA50519, R01 CA100710, R01 CA050519, R37 CA050519, CA100710] Funding Source: Medline
Damage recognition by repair/checkpoint factors is the critical first step of the DNA damage response. DNA double strand breaks ( DSBs) activate checkpoint signaling and are repaired by nonhomologous end-joining (NHEJ) and homologous recombination (HR) pathways. However, in vivo kinetics of the individual factor responses and the mechanism of pathway choice are not well understood. We report cell cycle and time course analyses of checkpoint activation by ataxia-telangiectasia mutated and damage site recruitment of the repair factors in response to laser-induced DSBs. We found that MRN acts as a DNA damage marker, continuously localizing at unrepaired damage sites. Damage recognition by NHEJ factors precedes that of HR factors. HR factor recruitment is not influenced by NHEJ factor assembly and occurs throughout interphase. Damage site retention of NHEJ factors is transient, whereas HR factors persist at unrepaired lesions, revealing unique roles of the two pathways in mammalian cells.
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