Homozygosity for the Minallele of Apc results in disruption of mouse development prior to gastrulation

Amy Rapaich Moser, Alex R. Shoemaker, Camille S. Connelly, Linda Clipson, Karen A. Gould, Cindy Luongo, William F. Dove, Pamela H. Siggers, Richard L. Gardner

Research output: Contribution to journalArticlepeer-review

132 Scopus citations


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. ©1995 Wiley‐Liss, Inc.

Original languageEnglish (US)
Pages (from-to)422-433
Number of pages12
JournalDevelopmental Dynamics
Issue number4
StatePublished - Aug 1995
Externally publishedYes


  • Apc
  • Conceptus
  • Mouse development
  • Postimplantation mutant
  • Primitive ectoderm
  • Tumor suppressor gene

ASJC Scopus subject areas

  • Developmental Biology


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