文献类型: 外文期刊
作者: Wang, Shifan 1 ; Guo, Huijuan 1 ; Zhu-Salzman, Keyan 3 ; Ge, Feng 1 ; Sun, Yucheng 1 ;
作者机构: 1.Chinese Acad Sci, Inst Zool, State Key Lab Integrated Management Pest Insects, Beijing 100101, Peoples R China
2.Univ Chinese Acad Sci, CAS Ctr Excellence Biot Interact, Beijing 100049, Peoples R China
3.Texas A&M Univ, Dept Entomol, College Stn, TX 77843 USA
4.Shandong Acad Agr Sci, Inst Plant Protect, Jinan 250100, Peoples R China
期刊名称:NATURE COMMUNICATIONS ( 影响因子:14.919; 五年影响因子:15.805 )
ISSN:
年卷期: 2022 年 13 卷 1 期
页码:
收录情况: SCI
摘要: Apoptosis and autophagy are two common forms of programmed cell death (PCD) used by host organisms to fight against virus infection. PCD in arthropod vectors can be manipulated by arboviruses, leading to arbovirus-vector coexistence, although the underlying mechanism is largely unknown. In this study, we find that coat protein (CP) of an insect-borne plant virus TYLCV directly interacts with a phosphatidylethanolamine-binding protein (PEBP) in its vector whitefly to downregulate MAPK signaling cascade. As a result, apoptosis is activated in the whitefly increasing viral load. Simultaneously, the PEBP4-CP interaction releases ATG8, a hallmark of autophagy initiation, which reduces arbovirus levels. Furthermore, apoptosis-promoted virus amplification is prevented by agonist-induced autophagy, whereas the autophagy-suppressed virus load is unaffected by manipulating apoptosis, suggesting that the viral load is predominantly determined by autophagy rather than by apoptosis. Our results demonstrate that a mild intracellular immune response including balanced apoptosis and autophagy might facilitate arbovirus preservation within its whitefly insect vector. Arbovirus has co-evolved with its insect vector, enabling efficient and persistent transmission by vectors. Here, the authors reveal an immune homeostatic mechanism shaped by apoptosis and autophagy that facilitates arbovirus preservation within its whitefly vector.
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