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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Maternal Nanos represses hid/skl-dependent apoptosis to maintain the germ line in Drosophila embryos
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Maternal Nanos represses hid/skl-dependent apoptosis to maintain the germ line in Drosophila embryos

机译:母体Nanos抑制hid / skl依赖性细胞凋亡以维持果蝇胚胎中的种系

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摘要

Nanos (Nos) is an evolutionary conserved protein essential for the survival of primordial germ cells. In Drosophila, maternal Nos partitions into pole cells and suppresses apoptosis to permit proper germ-line development. However, how this critical event is regulated by Nos has remained elusive. Here, we report that Nos represses apoptosis of pole cells by suppressing translation of head involution defective (hid), a member of the RHG gene family that is required for Caspase activation. In addition, we demonstrate that hid acts in concert with another RHG gene, sickle (skl), to induce apoptosis. Expression of skl is induced in pole cells by maternal tao-1, aste20-like serine/threonine kinase. Tao-1-dependent skl expression is required to potentiate hid activity. However, skl expression is largely suppressed in normal pole cells. Once the pole cells lack maternal Nos, Tao-1-dependent skl expression is fully activated, suggesting that skl expression is also restricted by Nos. These findings provide the first evidence that the germ line is maintained through the regulated expression of RHG genes.
机译:Nanos(Nos)是一种进化的保守蛋白,对于原始生殖细胞的存活至关重要。在果蝇中,母体Nos分裂成极细胞并抑制细胞凋亡,以允许适当的种系发育。但是,如何通过Nos来控制这一关键事件仍然难以捉摸。在这里,我们报道Nos通过抑制头对合缺陷(hid)的翻译来抑制极细胞的凋亡,hid缺陷是Caspase激活所需的RHG基因家族的成员。此外,我们证明了hid与另一个RHG基因镰刀(skl)协同作用,可诱导细胞凋亡。 sk1的表达是由母体tao-1,aste20样丝氨酸/苏氨酸激酶在极细胞中诱导的。 Tao-1依赖的skl表达是增强hid活动所必需的。然而,在正常极细胞中skl表达被大大抑制。一旦极细胞缺乏母体Nos,Tao-1依赖的skl表达就被完全激活,这表明skl表达也受到Nos的限制。这些发现为生殖系通过RHG基因的调控表达得以维持提供了第一个证据。

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