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Homozygosity for the Min allele of Apc results in disruption of mouse development prior to gastrulation
Author(s) -
Moser Amy Rapaich,
Shoemaker Alex R.,
Connelly Camille S.,
Clipson Linda,
Gould Karen A.,
Luongo Cindy,
Dove William F.,
Siggers Pamela H.,
Gardner Richard L.
Publication year - 1995
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/aja.1002030405
Subject(s) - biology , gastrulation , adenomatous polyposis coli , ectoderm , allele , embryo , trophoblast , phenotype , embryogenesis , genetics , mutation , microbiology and biotechnology , gene , cancer research , fetus , colorectal cancer , cancer , pregnancy , placenta
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 Apc Min ( 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.