| First Author | Moser AR | Year | 1995 |
| Journal | Dev Dyn | Volume | 203 |
| Issue | 4 | Pages | 422-33 |
| PubMed ID | 7496034 | Mgi Jnum | J:27993 |
| Mgi Id | MGI:75627 | Doi | 10.1002/aja.1002030405 |
| Citation | Moser AR, et al. (1995) Homozygosity for the Min allele of Apc results in disruption of mouse development prior to gastrulation. Dev Dyn 203(4):422-33 |
| abstractText | Mutation of the APC (adenomatous polyposis coli) gene is an early event in colon tumor development in humans. Mice carrying Min (multiple intestinal neoplasia), a mutant allele of Apc, develop intestinal and mammary tumors as adults. To study the role of the Apc gene in development, we have investigated the phenotype of embryos homozygous for ApcMin (Min). Development of the primitive ectoderm fails prior to gastrulation in homozygous Min embryos. By midgestation, the presumed homozygotes consist of a mass of trophoblast giant cells with an additional cluster of much smaller embryonic cells. These results indicate that functional Apc is required for normal growth of inner cell mass derivatives. |
