Disruption of Apc10/Doc1 in three alleles of Oligosyndactylism

被引：17

作者：

Pravtcheva, DD ^{[1
]}

Wise, TL ^{[1
]}

机构：

[1] New York State Inst Basic Res Dev Disabil, Dept Human Genet, Staten Isl, NY 10314 USA

来源：

GENOMICS | 2001年 / 72卷 / 01期

关键词：

D O I：

10.1006/geno.2001.6474

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

Oligosyndactylism (Os) is a radiation-induced mouse mutation associated with recessive lethality and a dominant effect on limb and kidney development. The lethal effect of the mutation is due to a cell-autonomous block in the transition from metaphase to anaphase. We have previously characterized two transgene-induced mutations, 94-A and 94-K, which are allelic with Os. These mutations facilitated the identification of genomic segments and transcribed sequences in the affected region. One of the transcripts in this region corresponds to the mouse homolog of the anaphase-promoting complex component APC10/DOC1. The disruption of this gene can explain the mitotic arrest phenotype of all three alleles of Os. (C) 2001 Academic Press.

引用

页码：78 / 87

页数：10

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