Translational repression of C. elegans p53 by GLD-1 regulates DNA damage-induced apoptosis

Björn Schumacher, Momoyo Hanazawa, Min Ho Lee, Sudhir Nayak, Katrin Volkmann, Randall Hofmann, Michael Hengartner, Tim Schedl, Anton Gartner

Research output: Contribution to journalArticlepeer-review

176 Scopus citations


p53 is a tumor suppressor gene whose regulation is crucial to maintaining genome stability and for the apoptotic elimination of abnormal, potentially cancer-predisposing cells. C. elegans contains a primordial p53 gene, cep-1, that acts as a transcription factor necessary for DNA damage-induced apoptosis. In a genetic screen for negative regulators of CEP-1, we identified a mutation in GLD-1, a translational repressor implicated in multiple C. elegans germ cell fate decisions and related to mammalian Quaking proteins. CEP-1-dependent transcription of proapoptotic genes is upregulated in the gld-1(op236) mutant and an elevation of p53-mediated germ cell apoptosis in response to DNA damage is observed. Further, we demonstrate that GLD-1 mediates its repressive effect by directly binding to the 3′UTR of cep-1/p53 mRNA and repressing its translation. This study reveals that the regulation of cep-1/p53 translation influences DNA damage-induced apoptosis and demonstrates the physiological importance of this mechanism.

Original languageEnglish
Pages (from-to)357-368
Number of pages12
Issue number3
StatePublished - Feb 11 2005


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