The C-elegans Myt1 ortholog is required for the proper timing of oocyte maturation
The C-elegans Myt1 ortholog is required for the proper timing of oocyte maturation
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DOI：
10.1242/dev.02241
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发表时间：
2006-02-01
期刊：
影响因子：
4.6
通讯作者：
Golden, A
中科院分区：
文献类型：
--
作者：
Burrows, AE;Sceurman, BK;Golden, A
成熟促进因子（MPF）是细胞周期蛋白依赖性激酶1和细胞周期蛋白B的复合物，在所有动物中驱动卵母细胞成熟。在卵母细胞成熟和受精之前，必须存在阻断MPF激活的机制以防止早熟细胞周期进展。本研究旨在确定受精前卵母细胞中早熟激活MPF的发育后果。而在爪蟾卵母细胞中的Myt 1的损耗导致核膜破裂在体外，我们发现，损耗的Myt 1的直系同源物WEE-1.3在线虫雌雄同体导致早熟的卵母细胞在体内成熟。虽然这些卵母细胞排卵，但它们不能受精。我们还观察到这些早熟卵母细胞的新表型，如染色体聚结，异常减数分裂纺锤体组织，和减数分裂II受精后标记的表达。此外，CDK-1和WEE-1.3的共耗竭研究表明，WEE-1.3在不存在CDK-1的情况下被抑制，这表明CDK-1是WEE-1.3在C.线虫卵母细胞
Maturation promoting factor (MPF), a complex of cyclin-dependent kinase 1 and cyclin B, drives oocyte maturation in all animals. Mechanisms to block MPF activation in developing oocytes must exist to prevent precocious cell cycle progression prior to oocyte maturation and fertilization. This study sought to determine the developmental consequences of precociously activating MPF in oocytes prior to fertilization. Whereas depletion of Myt1 in Xenopus oocytes causes nuclear envelope breakdown in vitro, we found that depletion of the Myt1 ortholog WEE-1.3 in C elegans hermaphrodites causes precocious oocyte maturation in vivo. Although such oocytes are ovulated, they are fertilization incompetent. We have also observed novel phenotypes in these precociously maturing oocytes, such as chromosome coalescence, aberrant meiotic spindle organization, and the expression of a meiosis II post-fertilization marker. Furthermore, co-depletion studies of CDK-1 and WEE-1.3 demonstrate that WEE-1.3 is dispensable in the absence of CDK-1, suggesting that CDK-1 is a major target of WEE-1.3 in C. elegans oocytes.