HOMOZYGOSITY FOR THE MIN ALLELE OF APC RESULTS IN DISRUPTION OF MOUSE DEVELOPMENT PRIOR TO GASTRULATION

被引:125
作者
MOSER, AR
SHOEMAKER, AR
CONNELLY, CS
CLIPSON, L
GOULD, KA
LUONGO, C
DOVE, WF
SIGGERS, PH
GARDNER, RL
机构
[1] UNIV WISCONSIN,MCARDLE LAB CANC RES,MADISON,WI 53706
[2] UNIV WISCONSIN,GENET LAB,MADISON,WI 53706
[3] UNIV OXFORD,DEV BIOL UNIT,IMPERIAL CANC RES FUND,OXFORD OX1 3PS,ENGLAND
关键词
PRIMITIVE ECTODERM; MOUSE DEVELOPMENT; TUMOR SUPPRESSOR GENE; APC; POSTIMPLANTATION MUTANT; CONCEPTUS;
D O I
10.1002/aja.1002030405
中图分类号
R602 [外科病理学、解剖学]; R32 [人体形态学];
学科分类号
100101 ;
摘要
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 Ape, develop intestinal and mammary tumors as adults. To study the role of the Ape 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 Ape is required for normal growth of inner cell mass derivatives. (C) 1995 Wiley-Liss, Inc.
引用
收藏
页码:422 / 433
页数:12
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