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首页> 外文期刊>Cell cycle >Reduced spermatogonial proliferation and decreased fertility in mice overexpressing cyclin E in spermatogonia.
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Reduced spermatogonial proliferation and decreased fertility in mice overexpressing cyclin E in spermatogonia.

机译：精原细胞中过度表达细胞周期蛋白E的小鼠精原细胞增殖减少和生育力降低。

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摘要

Cyclin E is a key component of the cell cycle regulatory machinery, contributing to the activation of Cdk2 and the control of cell cycle progression at several stages. Cyclin E expression is tightly regulated, by periodic transcription and ubiquitin-mediated degradation. Overexpression of cyclin E has been associated with tumor development and poor prognosis in several tumor types, including germ cell tumors and both cyclin E and its partner Cdk2 are required for normal spermatogenesis. Here we have generated and characterized transgenic mice overexpressing a cyclin E mutant protein, resistant to ubiquitin-mediated proteolysis, in testicular germ cells, under the control of the human EF-1alpha promoter. The transgenic mice develop normally and live a normal life span, with no signs of testicular tumor development. The transgenic mice display however reduced fertility and testicular atrophy, due to reduced spermatogonial proliferation as a consequence of deregulated cyclin E levels. Overall our results show that deregulation of cyclin E expression contribute to infertility, due to inability of the spermatogonial cells to start the mitotic cycles prior to entering meiosis.
机译：细胞周期蛋白E是细胞周期调节机制的关键组成部分，在多个阶段有助于Cdk2的活化和细胞周期进程的控制。细胞周期蛋白E的表达受到周期性转录和泛素介导的降解的严格调控。细胞周期蛋白E的过表达与多种肿瘤类型（包括生殖细胞肿瘤）的肿瘤发展和不良预后相关，细胞周期蛋白E及其伴侣Cdk2都是正常精子发生所必需的。在这里，我们已经生成并鉴定了在人EF-1alpha启动子的控制下，在睾丸生殖细胞中过表达细胞周期蛋白E突变蛋白，对泛素介导的蛋白水解有抗性的转基因小鼠。转基因小鼠正常发育，寿命正常，没有睾丸肿瘤发展的迹象。然而，由于细胞周期蛋白E水平失调，精原细胞的增殖减少，导致转基因小鼠的生育力和睾丸萎缩降低。总体而言，我们的结果表明，由于精原细胞在进入减数分裂之前无法启动有丝分裂周期，因此细胞周期蛋白E表达失调会导致不育。

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