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Rice ragged stunt virus Pns10 induces mitochondrial-mediated apoptosis to promote viral infection in Nilaparvata lugens through disrupting the NlNDUFS1-NlPHB2 interaction

文献类型： 外文期刊

作者： Zheng, Lianshun 1 ; Fu, Shuai 1 ; Zeng, Ming 1 ; Li, Liyan 1 ; Wang, Dan 1 ; Gao, Shibo 1 ; Zhang, Yunge 1 ; Zhang, Cui 1 ; Fei, Shifang 1 ; Ye, Xuan 1 ; Chen, Lele 1 ; Chen, Qianhui 1 ; Wang, Yaqin 1 ; Zhou, Xueping 1 ; Xie, Yan 1 ; Hu, Boli 5 ; Wu, Jianxiang 1 ;

作者机构： 1.Zhejiang Univ, Inst Biotechnol, State Key Lab Rice Biol & Breeding, Zhejiang Key Lab Biol & Ecol Regulat Crop Pathogen, Hangzhou, Zhejiang, Peoples R China

2.Zhejiang Univ, Hainan Inst, Sanya, Peoples R China

3.Zhejiang Lab, Res Ctr Life Sci Comp, Hangzhou, Peoples R China

4.Chinese Acad Agr Sci, Inst Plant Protect, State Key Lab Biol Plant Dis & Insect Pests, Beijing, Peoples R China

5.Zhejiang Univ, Ctr Vet Sci, MOA Key Lab Anim Virol, Hangzhou, Peoples R China

期刊名称：PLOS PATHOGENS （ 影响因子：4.9； 五年影响因子：5.4 ）

ISSN： 1553-7366

年卷期： 2025 年 21 卷 8 期

页码：

收录情况： SCI

摘要： Apoptosis, a programmed cell death process, plays crucial roles in host antiviral response. Although there are many reports on the relationship between cell apoptosis and viral infection, the mechanisms underlying plant arbovirus-induced apoptosis in insect vectors remain largely unclear. Here, we reported that apoptosis promotes rice ragged stunt virus (RRSV) infection in Nilaparvata lugens (brown planthopper), and RRSV-encoded Pns10 protein can induce apoptosis in N. lugens. The Pns10 interacts with N. lugens NADH:ubiquinone oxidoreductase 75 kDa Fe-S protein 1(NlNDUFS1), a core subunit of mitochondrial complex I. Silencing of NlNDUFS1 expression in N. lugens impaired mitochondrial complex I activity, decreasing ATP production and increasing mitochondrial ROS accumulation. This dysregulation triggers apoptosis to promote RRSV infection in N. lugens. Furthermore, RRSV Pns10 disrupts the interaction between NlNDUFS1 and NlProhibitin 2 (NlPHB2) in N. lugens to impair mitochondrial complex I activity, leading to a decrease of ATP production and an increase of mitochondrial ROS accumulation. The excessive accumulation of mitochondrial ROS causes genomic DNA fragmentation and apoptosis. Collectively, the findings presented here illuminate a novel mechanism by which a plant virus manipulates vector mitochondrial apoptosis to benefit viral infection, and offer insights for future transmission-blocking interventions.

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