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.