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Updated: May 3, 2026

Computational Analysis of the Caenorhabditis elegans Germline to Study the Distribution of Nuclei, Proteins, and the Cytoskeleton
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Translational repression of C. elegans p53 by GLD-1 regulates DNA damage-induced apoptosis

Björn Schumacher1, Momoyo Hanazawa, Min-Ho Lee

  • 1Department of Cell Biology, Max-Planck-Institute for Biochemistry, Am Klopferspitz 18a, D 82152 Martinsried, Germany.

Cell
|February 15, 2005
PubMed

Insights

The tumor suppressor p53 (encoded by cep-1 in C. elegans) is regulated by GLD-1, a protein that represses its translation. This regulation is vital for DNA damage-induced apoptosis and maintaining genome stability.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • p53 is a critical tumor suppressor gene regulating genome stability and apoptosis.
  • The C. elegans homolog of p53, cep-1, is essential for DNA damage-induced apoptosis.
  • Understanding p53 regulation is key to cancer prevention and treatment.

Purpose of the Study:

  • To identify novel regulators of CEP-1 function in C. elegans.
  • To investigate the role of translational control in DNA damage response pathways.
  • To elucidate the mechanism by which GLD-1 affects CEP-1 activity and apoptosis.

Main Methods:

  • Genetic screening in C. elegans to identify CEP-1 regulators.
  • Analysis of gene expression and protein translation using molecular assays.
  • RNA-binding assays to confirm direct interaction between GLD-1 and cep-1 mRNA.

Main Results:

  • A mutation in GLD-1, a translational repressor, was identified as a negative regulator of CEP-1.
  • CEP-1-dependent transcription of proapoptotic genes and germ cell apoptosis were upregulated in gld-1 mutants.
  • GLD-1 directly binds to the 3'UTR of cep-1 mRNA, repressing its translation.

Conclusions:

  • GLD-1 negatively regulates CEP-1/p53 translation, impacting DNA damage-induced apoptosis.
  • Translational control of cep-1/p53 is a significant mechanism for modulating apoptosis.
  • This study highlights the physiological importance of translational regulation in maintaining genome stability.

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