Abstract
Double-strand breaks (DSBs) constitute the most dangerous DNA damage. Nonetheless, besides unwanted DSBs that continuously arise, for example, upon reactive oxygen species or ionizing radiation, hematopoietic B and T cells undergo programmed DSBs during V(D)J and class switch recombination (CSR) to tailor antigen-specific antibodies and T-cell receptor. To maintain genomic stability, an immediate and faithful repair of DSBs is absolutely required. Nonhomologous end joining (NHEJ) is the main DNA DSB-repair pathway in cells that directly rejoins DSBs without template. Recently, there are growing evidences that NHEJ consists of two pathways: the alternative and classical NHEJ. The latter is faithful and guarantees genomic stability, whereas alternative NHEJ is mutagenic and causes chromosomal aberration. Here, both pathways and their components in mammals are introduced emphasizing their function, structure, binding partners, and possible regulation. The role of NHEJ in context of V(D)J and CSR is also discussed.
Published Version
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