ATM is required for efficient recombination between immunoglobulin switch regions.

Date publication

novembre 2004

Auteurs

Membres identifiés du Cancéropôle Est :
Dr REINA-SAN-MARTIN Bernardo

Tous les auteurs :
Reina-San-Martin B, Chen HT, Nussenzweig A, Nussenzweig MC

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/15520243

Résumé

Ataxia telangiectasia mutated (ATM) kinase is critical for initiating the signaling pathways that lead to cell cycle checkpoints and DNA double strand break repair. In the absence of ATM, humans and mice show a primary immunodeficiency that includes low serum antibody titers, but the role of ATM in antigen-driven immunoglobulin gene diversification has not been defined. Here, we show that although ATM is dispensable for somatic hypermutation, it is required for efficient class switch recombination (CSR). The defect in CSR is not due to alterations in switch region transcription, accessibility, DNA damage checkpoint protein recruitment, or short-range intra-switch region recombination. Only long-range inter-switch recombination is defective, indicating an unexpected role for ATM in switch region synapsis during CSR.

Référence

J Exp Med. 2004 Nov 1;200(9):1103-10.