Homologue disjunction in mouse oocytes requires proteolysis of securin and cyclin B1

被引：164

作者：

Herbert, M

Levasseur, M

Homer, H

Yallop, K

Murdoch, A

McDougall, A

机构：

[1] Int Ctr Life, Biosci Ctr, Sch Surg & Reprod Sci, Cell & Dev Physiol Res Grp, Newcastle Upon Tyne NE1 4EP, Tyne & Wear, England

[2] Med Sch Newcastle Upon Tyne, Sch Cell & Mol Biosci, Cell & Dev Physiol Res Grp, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England

[3] Int Ctr Life, Biosci Ctr, Newcastle Fertil Ctr, Newcastle Upon Tyne NE1 4EP, Tyne & Wear, England

来源：

NATURE CELL BIOLOGY | 2003年 / 5卷 / 11期

关键词：

D O I：

10.1038/ncb1062

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Disjunction of pairs of homologous chromosomes during the first meiotic division (MI) requires anaphase-promoting complex (APC)-mediated activation of separase in budding yeast(1,2) and Caenorhabditis elegans(3,4,5), but not Xenopus laevis(6,7). It is not clear which model best fits the mammalian system. Here we show that homologue disjunction in mouse oocytes is dependent on proteolysis of the separase inhibitor securin and the Cdk1 regulatory sub-unit cyclin B1. Proteolysis of both proteins was entirely dependent on their conserved destruction box (D-box) motifs, through which they are targeted to the APC(8). These data indicate that the mechanisms regulating homologue disjunction in mammalian oocytes are similar to those of budding yeast and C. elegans.

引用

页码：1023 / 1025

页数：3

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