Ins and outs of meiosis in ascidians.
Ins and outs of meiosis in ascidians.
复制标题
海鞘减数分裂的来龙去脉。
DOI：
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发表时间：
1998
影响因子：
7.3
通讯作者：
B. Dale
中科院分区：
文献类型：
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作者：
G. Russo;M. Wilding;M. Marino;B. Dale
海鞘卵母细胞在第一次减数分裂的中期（M）被阻断。受精触发减数分裂的完成而没有任何进一步的停滞。在这篇综述中，我们分析了这些卵母细胞减数分裂进程的调控机制。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IP 3和CICR途径诱导细胞内钙释放，并通过触发ADP核糖（ADPr）的产生来门控受精电流。在M-I释放时观察到的MPF失活不需要钙振荡;然而，ADPr可能间接参与MPF相关激酶Cdc 2的活性。MPF活性在M-II达到第二个峰，随后失活。进展为M-II依赖于细胞内钙振荡。MAP激酶（MAPK）活性在M-I退出时降低，并在减数分裂完成期间保持低水平。最后，虽然Cdc 2、Cyclin B和MAPK样蛋白已在海鞘卵母细胞中被鉴定，但CSF的组分仍有待鉴定。
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.