Two zinc finger proteins, OMA-1 and OMA-2, are redundantly required for oocyte maturation in C-elegans

Two zinc finger proteins, OMA-1 and OMA-2, are redundantly required for oocyte maturation in C-elegans
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DOI:
10.1016/s1534-5807(01)00026-0
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发表时间:
2001-08-01
期刊:
影响因子:
11.8
通讯作者:
Lin, RL
Lin, RL
中科院分区:
生物学1区
文献类型:
--
作者:
Detwiler, MR;Reuben, M;Lin, RL

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卵母细胞通过称为卵母细胞成熟的过程从减数分裂前期 I 停滞中释放出来。我们在这里展示了卵母细胞成熟的遗传特征,使用秀丽隐杆线虫作为模型系统。我们发现两种 TIS11 含锌指蛋白 OMA-1 和 OMA-2 在成熟卵母细胞中特异性表达,并在卵母细胞成熟过程中发挥冗余作用。 oma-1;oma-2 突变体中的卵母细胞启动但未完成成熟,并在前期 1 的某个特定点处停滞。Oma 卵母细胞中不会发生两种成熟信号诱导的分子事件,包括激活 MAP 激酶的维持。 Oma 前期停滞是通过 MYT-1 样激酶失活而释放的,表明 OMA-1 和 OMA-2 在 MYT-1 上游发挥作用,作为减数分裂成熟过程中前期进展的正调节因子。
Oocytes are released from meiotic prophase I arrest through a process termed oocyte maturation. We present here a genetic characterization of oocyte maturation, using C. elegans as a model system. We show that two TIS11 zinc finger-containing proteins, OMA-1 and OMA-2, express specifically in maturing oocytes and function redundantly in oocyte maturation. Oocytes in oma-1;oma-2 mutants initiate but do not complete maturation and arrest at a defined point in prophase 1. Two maturation signal-induced molecular events, including the maintenance of activated MAP kinase, do not occur in Oma oocytes. The Oma prophase arrest is released by inactivation of a MYT-1-like kinase, suggesting that OMA-1 and OMA-2 function upstream of MYT-1 as positive regulators of prophase progression during meiotic maturation.