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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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

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.[1]

References

  1. Translational repression of C. elegans p53 by GLD-1 regulates DNA damage-induced apoptosis. Schumacher, B., Hanazawa, M., Lee, M.H., Nayak, S., Volkmann, K., Hofmann, E.R., Hofmann, R., Hengartner, M., Schedl, T., Gartner, A. Cell (2005) [Pubmed]
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