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p53 is a transcription factor that regulates the response to cellular stress. Mammalian p53 functions as a tumor suppressor. The  C. elegans  p53,  cep-1 , regulates DNA-damage induced germline cell death by activating the transcription of  egl-1  and  ced-13 . We used the  C. elegans  model to investigate how, in the whole animal, different forms of DNA damage can induce p53-dependent versus p53-independent cell death and DNA repair. DNA damage was induced by ultraviolet type C (UVC) radiation, or 10-decarbamoyl mitomycin C (DMC, an agent known to induce mammalian p53-independent cell death). Wild-type or  cep-1  loss-of-function mutant animals were assayed for germline cell death and DNA lesions. Wild-type animals displayed greater removal of UVC-lesions over time, whereas  cep-1  mutant animals displayed increased UVC-lesion retention. The  cep-1  mutation increased UVC-lesion retention directly correlated with a reduction of progeny viability. Consistent with DMC inducing p53-independent cell death in mammalian cells DMC induced a  C. elegans  p53-independent germline cell death pathway. To examine the influence of wild-type CEP-1 and DNA damage on  C. elegans  tumors we used  glp-1(ar202gf)/Notch  germline tumor mutants. UVC treatment of  glp-1  mutant animals activated the CEP-1 target gene  egl-1  and reduced tumor size. In  cep-1(gk138);glp-1(ar202gf)  animals, UVC treatment resulted in increased susceptibility to lesions and larger tumorous germlines. Interestingly, the partial knockdown of  bec-1  in adults resulted in a CEP-1-dependent increase in germline cell death and an increase in DNA damage. These results strongly support cross-talk between BEC-1 and CEP-1 to protect the  C. elegans  genome.

C. elegans CEP-1/p53 and BEC-1 Are Involved in DNA Repair