| Modification Notes |
p53, a DNA-binding, oligomerization domain- and transcription activation domain-containing tumor suppressor, upregulates growth arrest and apoptosis-related genes in response to stress signals, thereby influencing programmed cell death, cell differentiation and cell cycle control mechanisms. Cep-1 (p53-like protein), is the 644 amino acid C. elegans homolog of mammalian tumor suppressor p53. While the DNA binding domains of p53 and cep-1 share little homology, both recognize nearly identical DNA sequences. Ubiquitously expressed in embryos, cep-1 is required to activate apoptosis of germ cells in response to genotoxic stress, and additionally activates C. elegans pgh-1, the homolog of Gas1 (growth arrest-specific 1). Together, cep-1 and pgh-1 mediate embryonic viability of mutations of TELO2, which is an essential gene in the regulation of checkpoint responses. Overexpression of cep-1 has been found to cause widespread caspase-independent cell death. |
