Sensing of intermediates in V(D)J recombination by ATM

Eric J. Perkins, Ayyappan Nair, Dale O. Cowley, Terry Van Dyke, Yung Chang, Dale A. Ramsden

Research output: Contribution to journalArticle

99 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)159-164
Number of pages6
JournalGenes and Development
Volume16
Issue number2
DOIs
StatePublished - Jan 15 2002

Keywords

  • Checkpoint
  • DNA repair
  • DNA-PK
  • Doublestrand break
  • P53
  • RAG1

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology

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    Perkins, E. J., Nair, A., Cowley, D. O., Van Dyke, T., Chang, Y., & Ramsden, D. A. (2002). Sensing of intermediates in V(D)J recombination by ATM. Genes and Development, 16(2), 159-164. https://doi.org/10.1101/gad.956902