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Significance Classical nonhomologous end joining (C-NHEJ) is a major mammalian DNA double–strand break (DSB) repair pathway. During V(D)J recombination in progenitor (pro)-B lymphocytes, C-NHEJ joins programmed DSBs in antibody gene loci to form complete antibody genes. C-NHEJ also protects mammalian cells from the harmful effects of exposure to ionizing radiation. We now find that the recently identified paralogue of XRCC4 and XLF (PAXX) DNA repair factor, like the related XLF repair factor, is dispensable for V(D)J recombination. However, combined loss of these two factors in pro–B-cell lines totally abrogates V(D)J recombination DSB joining and greatly sensitizes the cells to ionizing radiation. These findings show that PAXX can provide critical C-NHEJ functions that are normally masked by functional redundancy with XLF.

PAXX and XLF DNA repair factors are functionally redundant in joining DNA breaks in a G1-arrested progenitor B-cell line