Journal
GENES & DEVELOPMENT
Volume 16, Issue 2, Pages 159-164Publisher
COLD SPRING HARBOR LAB PRESS
DOI: 10.1101/gad.956902
Keywords
checkpoint; DNA-PK; RAG1; p53; DNA repair; double-strand break
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Funding
- NCI NIH HHS [CA 84442-01, R01 CA084442] Funding Source: Medline
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Ataxia-telangiectasia mutated (ATM) is required for resistance to radiation-induced DNA breaks. Here we use chromatin immunoprecipitation to show that ATM also localizes to breaks associated with V(D)J recombination. ATM recruitment to the recombining locus correlates approximately with recruitment of the break-initiating factor RAG1 and precedes efficient break repair, consistent with localization of ATM to normal recombination intermediates. A product of ATM kinase activity, Ser 18-phosphorylated p53, was detected similarly at these breaks, arguing that ATM phosphorylates target proteins in situ. We suggest routine surveillance of intermediates in V(D)J recombination by ATM helps suppress potentially oncogenic translocations when repair fails.
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