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海鞘减数分裂的来龙去脉

Ins and outs of meiosis in ascidians.

作者信息

Russo G L, Wilding M, Marino M, Dale B

机构信息

Institute of Food Science and Technology, National Research Council, Avellino, 83100, Italy.

出版信息

Semin Cell Dev Biol. 1998 Oct;9(5):559-67. doi: 10.1006/scdb.1998.0250.

Abstract

Ascidian oocytes are blocked in metaphase (M) of the first meiotic division. Fertilization triggers the completion of meiosis without any further arrest. In this review, we have analyzed the mechanisms that regulate the progression through meiosis in these oocytes. A primary signal from the fertilizing spermatozoon, probably soluble sperm factor(s), induces intracellular calcium release by activating the IP3 and CICR pathways and gates the fertilization current by triggering the generation of ADP ribose (ADPr). The calcium oscillations are not required for the inactivation of MPF observed at M-I release; however, ADPr may be indirectly involved in the activity of MPF associated kinase, Cdc2. MPF activity reaches a second peak at M-II followed by subsequent inactivation. Progression to M-II is dependent on the intracellular calcium oscillations. MAP kinase (MAPK) activity decreases at M-I exit and remains low during the completion of meiosis. Finally, although Cdc2, Cyclin B and MAPK-like proteins have been identified in ascidian oocytes, components of CSF still remain to be identified.

摘要

海鞘卵母细胞停滞于第一次减数分裂的中期(M期)。受精触发减数分裂的完成,且不再有进一步的停滞。在本综述中,我们分析了调控这些卵母细胞减数分裂进程的机制。来自受精精子的主要信号,可能是可溶性精子因子,通过激活IP3和CICR途径诱导细胞内钙释放,并通过触发ADP核糖(ADPr)的生成来控制受精电流。在M-I期释放时观察到的MPF失活并不需要钙振荡;然而,ADPr可能间接参与与MPF相关的激酶Cdc2的活性。MPF活性在M-II期达到第二个峰值,随后失活。向M-II期的进展依赖于细胞内钙振荡。MAP激酶(MAPK)活性在M-I期退出时降低,并在减数分裂完成过程中保持较低水平。最后,尽管在海鞘卵母细胞中已鉴定出Cdc2、细胞周期蛋白B和MAPK样蛋白,但细胞静止因子(CSF)的成分仍有待确定。

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