| Literature DB >> 6091901 |
Abstract
The mutation, oligosyndactyly, results in syndactyly, muscle anomalies, and diabetes insipidus in heterozygous mice. When homozygous, the mutation is lethal early in development. Although homozygous embryos are able to form blastocyst outgrowths (the in vitro equivalent to implantation), cells begin to accumulate in mitosis as early as the blastocyst stage. Even though the cytologic appearance is that of mitotic cells treated with a microtubule inhibitor such as colcemid, the homozygous embryos do, in fact, have normal appearing mitotic spindles. These results define the Os mutation as one which, in the homozygous state, prevents the movement of chromosomes from the metaphase plate. It is the first mammalian developmental mutation to be so defined and is unique among all mitotic arrest mutations thus far described in higher eucaryotes.Entities:
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Year: 1984 PMID: 6091901 DOI: 10.1016/0092-8674(84)90277-0
Source DB: PubMed Journal: Cell ISSN: 0092-8674 Impact factor: 41.582