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53BP1 contributes to activation of the G2/M checkpoint downstream of ATM and MDC1 in response to ionizing radiation and promotes nonhomologous end-joining (NHEJ) in mammalian cells. In order to determine whether the cellular activities of 53BP1 are conserved in the model organism  C. elegans , we analyzed the function of its homolog, HSR-9 in response to DNA damage. Deletion or  Mos1 -insertion in  hsr-9  did not affect the sensitivity of worms to double strand DNA breaks (DSBs), as reflected in embryonic survival and larval development. Nevertheless, the  hsr-9  mutations, as well as a  lig-4  deletion, reversed the hypersensitivity of  rad-54 -deficient worms to DSBs. In addition, oocyte chromosomal aberrations, which were increased by  rad-54  knockdown in response to DSBs, were also reduced by the  hsr-9  mutations. The  hsr-9  mutations did not prevent the cell cycle arrest induced by DSBs in mitotically proliferating germ cells. However, they attenuated apoptosis induced by DSBs, but not when CEP-1 (a p53 ortholog) was absent, suggesting that HSR-9 functions in the same pathway as CEP-1. We concluded that the 53BP1 homolog in  C. elegans  is not directly involved in cell cycle arrest in response to DSBs, but that it promotes apoptosis and also a form of NHEJ that occurs only when  rad-54  is deficient.

The 53BP1 Homolog in C. elegans Influences DNA Repair and Promotes Apoptosis in Response to Ionizing Radiation