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双色绿僵菌寄生促进亲环素D与p53相互作用,诱导斜纹夜蛾血细胞凋亡。

Microplitis bicoloratus parasitism promotes cyclophilin D-p53 interaction to induce apoptosis of hemocytes in Spodoptera litura.

作者信息

Zhang Pan, Liu Zi-Yan, Yu Dan, Xu Cui-Xian, Hu Yan, Liang Ya-Ping, Jin Jie, Li Ming

机构信息

Key Laboratory of the University in Yunnan Province for International Cooperation in Intercellular Communications and Regulation, School of Life Sciences, Yunnan University, Kunming, China.

Center of Molecular Biology of Tropical Crops, Yunnan Institute of Tropical Crops, Jinghong, China.

出版信息

Arch Insect Biochem Physiol. 2023 Feb;112(2):e21970. doi: 10.1002/arch.21970. Epub 2022 Oct 6.

Abstract

Microplitis bicoloratus parasitism can induce apoptosis of hemocytes in the M. bicolortus host, Spodoptera litura. However, it is unclear how M. bicolortus parasitism regulates host signaling pathways to induce apoptosis. Expression of cyclophilin D (CypD) and p53 was significantly upregulated in S. litura hemocytes at 6 days postparasitization. In the parasitized hemocytes, there was mitochondrial membrane potential (△Ψ ) loss, cytochrome c (Cyt C) release from mitochondria, and caspase-3 activation. These occurred while hemocytes were undergoing upregulation of CypD and p53. Parasitism also promoted the interaction between CypD and p53. CypD silencing could rescue the apoptotic phenotypes induced by parasitism, but had no effect on apoptosis in unparasitized S. litura. These findings suggest that the CypD-p53 pathway may be an important component of the parasitism-induced immunosuppressive response and establish a basis for further studies of parasitoid/host interactions.

摘要

双色绿茧蜂寄生可诱导其寄主斜纹夜蛾血细胞凋亡。然而,尚不清楚双色绿茧蜂寄生如何调节寄主信号通路以诱导凋亡。寄生后6天,斜纹夜蛾血细胞中环孢素D(CypD)和p53的表达显著上调。在被寄生的血细胞中,线粒体膜电位(△Ψ)丧失,细胞色素c(Cyt C)从线粒体释放,且半胱天冬酶-3被激活。这些现象发生在血细胞中CypD和p53上调之时。寄生还促进了CypD与p53之间的相互作用。沉默CypD可挽救由寄生诱导的凋亡表型,但对未被寄生的斜纹夜蛾的凋亡无影响。这些发现表明,CypD-p53通路可能是寄生诱导的免疫抑制反应的重要组成部分,并为进一步研究寄生蜂/寄主相互作用奠定了基础。

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