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

AUTOR(ES)

Perkins, Eric J.

FONTE

Cold Spring Harbor Laboratory Press

RESUMO

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.

Documentos Relacionados

• Critical role for Atm in suppressing V(D)J recombination-driven thymic lymphoma
• Regulation of V(D)J Recombination by Transcriptional Promoters
• Postcleavage Sequence Specificity in V(D)J Recombination
• V(D)J recombination intermediates and non-standard products in XRCC4-deficient cells.
• RAG-Mediated V(D)J Recombination Is Not Essential for Tumorigenesis in Atm-Deficient Mice