First Author | Evans SC | Year | 2004 |
Journal | Mamm Genome | Volume | 15 |
Issue | 6 | Pages | 415-23 |
PubMed ID | 15181534 | Mgi Jnum | J:97137 |
Mgi Id | MGI:3574582 | Doi | 10.1007/s00335-004-2327-y |
Citation | Evans SC, et al. (2004) A novel genetic modifier of p53, mop1, results in embryonic lethality. Mamm Genome 15(6):415-23 |
abstractText | The heterogeneity that occurs in the tumor spectrum and latency in Li-Fraumeni syndrome (LFS) patients with inherited mutations in p53 suggest risk modifiers at loci other than the major gene. We developed a mouse model to investigate these risk modifiers. Inbred CE/J mice, which succumb to multiple types of tumors similar to those found in LFS, were crossed with the p53-null 129/Sv (129-Trp53(tm1Tyj)) mouse. In this cross, we uncovered evidence for a genetic modifier of p53, mop1, based on an unexpected mix of genotypes in the F2 progeny from Mendelian expectations. A model in which a recessive CE/J allele in combination with p53 heterozygosity or homozygosity results in lethality most closely fits the data. Using simple-sequence length polymorphism analysis of the entire genome, we identified a putative chromosomal region for this modifier of p53 on mouse chromosome 11 centromeric to p53. |