| First Author | Van Nostrand JL | Year | 2017 |
| Journal | Cell Death Differ | Volume | 24 |
| Issue | 4 | Pages | 575-579 |
| PubMed ID | 28211873 | Mgi Jnum | J:261303 |
| Mgi Id | MGI:6151196 | Doi | 10.1038/cdd.2016.128 |
| Citation | Van Nostrand JL, et al. (2017) The p53 family members have distinct roles during mammalian embryonic development. Cell Death Differ 24(4):575-579 |
| abstractText | The p53 tumor suppressor is a member of a multi-protein family, including the p63 and p73 transcription factors. These proteins can bind to the same consensus sites in DNA and activate the same target genes, suggesting that there could be functional redundancy between them. Indeed, double mutant mice heterozygous for any two family member-encoding genes display enhanced cancer phenotypes relative to single heterozygous mutants. However, whether the family members play redundant roles during embryonic development has remained largely unexplored. Although p53(-/-); p73(-/-) mice are born and manifest phenotypes characteristic of each of the single mutants, the consequences of combined deficiency of p63 and either p53 or p73 have not been elucidated. To examine the functional overlap of p53 family members during development, we bred and analyzed compound mutant embryo phenotypes. We discovered that double knockout embryos and five allele knockout embryos only displayed obvious defects accounted for by loss of single p53 family members. Surprisingly, at mid-gestation (E11), we identified a single viable triple knockout embryo that appeared grossly normal. Together, these results suggest that the p53 family is not absolutely required for early embryogenesis and that p53 family members are largely non-redundant during early development. |
