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首页> 外文期刊>Archives of Insect Biochemistry and Physiology >Identification of beta-chain of FoF1-ATPase in apoptotic cell population induced by Microplitis bicoloratus bracovirus and its role in the development of Spodoptera litura
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Identification of beta-chain of FoF1-ATPase in apoptotic cell population induced by Microplitis bicoloratus bracovirus and its role in the development of Spodoptera litura

机译:鉴定微观炎诱导的凋亡细胞群中FOF1-ATP酶的β链及其在Spodoptera Litura发育中的作用

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Two physiological changes of Spodoptera litura parasitized by Microplitis bicoloratus are hemocyte-apoptosis and retarded immature development. beta-Chain of FoF1-ATPase was found from a S. litura transcriptome. It belongs to a conserved P-loop NTPase superfamily, descending from a common ancestor of Lepidopteran clade. However, the characterization of beta-chain of ATPase in apoptotic cells and its involvement in development remain unknown. Here, the ectopic expression and endogenous FoF1-ATPase beta-chain occurred on S. litura cell membrane: in vivo, at the late stage of apoptotic hemocyte, endogenous FoF1-ATPase beta-chain was stably expressed during M. bicoloratus larva development from 4 to 7 days post-parasitization; in vitro, at an early stage of pre-apoptotic Spli221 cells by infecting with M. bicoloratus bracovirus particles, the proteins were speedily recover expression. Furthermore, endogenous FoF1-ATPase beta-chain was localized on the apoptotic cell membrane. RNA interference (RNAi) of FoF1-ATPase beta-chain led to significantly decreased head capsule width. This suggested that FoF1-ATPase beta-chain positively regulated the development of S. litura. The RNAi effect on the head capsule width was enhanced with parasitism. Our research found that FoF1-ATPase beta-chain was expressed and localized on the cell membrane in the apoptotic cells, and involved in the development of S. litura.
机译:微观菌寄生术寄生的SPODOPTERA LITURA的两种生理变化是血液细胞凋亡和延迟未成熟发育。从S. Litura转录组中发现FOF1-ATP酶的β链。它属于保守的P环NTPase Superfamily,从鳞翅目植物的共同祖先下降。然而,凋亡细胞中ATP酶的β链表征及其在发展中的参与仍然未知。在此,在S. litura细胞膜中发生异位表达和内源FOF1-ATP酶β-链:在体内,在凋亡血细胞晚期,内源FOF1-ATP酶β-链在4时稳定地表达4μl寄生后7天;在体外,通过用M.Bicoloratus Bracovirus颗粒感染前凋亡紫草菌细胞的早期阶段,蛋白质迅速回收表达。此外,内源FOF1-ATPaseβ链在凋亡细胞膜上局部化。 FOF1-ATPaseβ-链的RNA干扰(RNAi)导致头部胶囊宽度显着降低。这表明FOF1-ATPaseβ链积极地调节S. Litura的发展。用寄生刺激增强了对头部胶囊宽度的RNAi效应。我们的研究发现,在凋亡细胞中的细胞膜上表达和定位FOF1-ATPaseβ链,并参与S. Litura的发育。

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