The Double-Edged Sword of Activation-Induced Cytidine Deaminase | Zendy

Xiaosheng Wu | Zendy; Pedro Geraldes | Zendy; Jeffrey L. Platt | Zendy; Marília Cascalho | Zendy

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The Double-Edged Sword of Activation-Induced Cytidine Deaminase

Author(s) -

Xiaosheng Wu,

Pedro Geraldes,

Jeffrey L. Platt,

Marília Cascalho

Publication year - 2005

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.174.2.934

Subject(s) - cytidine deaminase , activation induced (cytidine) deaminase , cytidine , dna , microbiology and biotechnology , deamination , biology , dna damage , mutant , immunoglobulin class switching , genetics , biochemistry , enzyme , b cell , gene , antibody

Activation-induced cytidine deaminase (AID) is required for Ig class switch recombination, a process that introduces DNA double-strand breaks in B cells. We show in this study that AID associates with the DNA-dependent protein kinase catalytic subunit (DNA-PKcs) promoting cell survival, presumably by resolving DNA double-strand breaks. Wild-type cells expressing AID mutants that fail to associate with DNA-PKcs or cells deficient in DNA-PKcs or 53BP1 expressing wild-type AID accumulate gammaH2AX foci, indicative of heightened DNA damage response. Thus, AID has two independent functions. AID catalyzes cytidine deamination that originates DNA double-strand breaks needed for recombination, and it promotes DNA damage response and cell survival. Our results thus resolve the paradox of how B cells undergoing DNA cytidine deamination and recombination exhibit heightened survival and suggest a mechanism for hyperIgM type II syndrome associated with AID mutants deficient in DNA-PKcs binding.

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