Molecular mechanisms utilized by alternative c-kit gene products in the control of spermatogonial proliferation and sperm-mediated egg activation
Molecular mechanisms utilized by alternative c-kit gene products in the control of spermatogonial proliferation and sperm-mediated egg activation
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DOI：
10.1046/j.1439-0272.2003.00539.x
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发表时间：
2003-02-01
期刊：
影响因子：
2.4
通讯作者：
Geremia, R
中科院分区：
文献类型：
--
作者：
Rossi, P;Dolci, S;Geremia, R
c-kit原癌基因通过两种可选择的基因产物在小鼠雄性生育力的控制中起双重作用：（1）c-kit [跨膜酪氨酸激酶干细胞因子受体（SCF）]，其在出生后睾丸的精原细胞分化中表达和起作用，其中c-kit是减数分裂前增殖所必需的;和（2）tr-kit，一种细胞内蛋白，其通过使用替代内含子启动子在精子发生期间特异性积累，并且当显微注射到中期II停滞的卵母细胞的细胞质中时能够触发小鼠卵活化。在这里，我们总结了最新的研究结果，通过c-kit调节细胞周期进程的有丝分裂生殖细胞的分子途径，并通过精子衍生的tr-kit触发孤雌完成减数分裂II和原核形成显微注射小鼠卵。
The c-kit proto-oncogene plays a dual role in the control of male fertility in mice through two alternative gene products: (1) c-kit [the transmembrane tyrosine kinase receptor for stem cell factor (SCF)], which is expressed and functional in differentiating spermatogonia of the postnatal testis, in which c-kit is essential for pre-meiotic proliferation; and (2) tr-kit, an intracellular protein which is specifically accumulated during spermiogenesis through the use of an alternative intronic promoter, and which is able to trigger mouse egg activation when microinjected into the cytoplasm of metaphase II arrested oocytes. Here, we summarize the most recent findings about the molecular pathways through which c-kit regulates cell cycle progression in mitotic germ cells, and those through which sperm-derived tr-kit triggers parthenogenetic completion of meiosis II and pronuclear formation in microinjected mouse eggs.