The JAK-STAT pathway promotes persistent viral infection by activating apoptosis in insect vectors.
The JAK-STAT pathway promotes persistent viral infection by activating apoptosis in insect vectors.
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JAK-STAT通路通过激活昆虫载体的细胞凋亡促进病毒的持续感染。
DOI：
10.1371/journal.ppat.1011266
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发表时间：
2023-03
期刊：
影响因子：
6.7
通讯作者：
中科院分区：
文献类型：
--
作者：
Janus激酶-信号转导子和转录激活子（JAK-STAT）通路是一种进化上保守的信号通路，可以调节多种生物学过程。然而，JAK-STAT信号通路在昆虫媒介病毒持续感染中的作用却很少被研究。本研究利用水稻条纹病毒（Rice stripe virus，RSV）和水稻黑条矮缩病毒（Rice black-streaked dwarf virus，RBSDV）及其昆虫载体小褐飞虱（Small brown planthopper）构建的系统，阐明了JAK-STAT途径在病毒持续侵染中的调控机制。RSV和RBSDV感染均激活JAK-STAT途径，并促进细胞因子信号转导抑制因子5（SOCS 5）的积累，SOCS 5是一种受转录因子STAT 5 B调控的E3泛素连接酶。有趣的是，病毒诱导的SOCS 5直接与抗凋亡B细胞淋巴瘤-2（BCL 2）相互作用，通过26 S蛋白酶体途径加速BCL 2的降解。因此，细胞凋亡的激活促进了其载体中的持续病毒感染。此外，STAT 5 B激活促进病毒扩增，而STAT 5 B抑制抑制细胞凋亡和减少病毒积累。综上所述，我们的研究结果揭示了病毒诱导的JAK-STAT途径通过调控细胞凋亡促进病毒感染，揭示了JAK-STAT途径在节肢动物介导的植物病毒持续传播中的新的调控机制。Janus激酶-信号转导子和转录激活子（JAK-STAT）途径在哺乳动物中作为先天性抗病毒免疫，而其在昆虫载体持续传播植物病毒中的作用在很大程度上仍然未知。在这项研究中，我们报告了植物病毒感染激活JAK-STAT途径，该途径调节细胞凋亡，以利于病毒在昆虫载体中的积累。这是持续性病毒感染中病毒诱导细胞凋亡的一种新的调控机制。此外，我们的新发现极大地扩展了我们对JAK-STAT和其他途径之间复杂串扰的了解，以促进病毒在昆虫载体中的持续传播。
The Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway is an evolutionarily conserved signaling pathway that can regulate various biological processes. However, the role of JAK-STAT pathway in the persistent viral infection in insect vectors has rarely been investigated. Here, using a system that comprised two different plant viruses, Rice stripe virus (RSV) and Rice black-streaked dwarf virus (RBSDV), as well as their insect vector small brown planthopper, we elucidated the regulatory mechanism of JAK-STAT pathway in persistent viral infection. Both RSV and RBSDV infection activated the JAK-STAT pathway and promoted the accumulation of suppressor of cytokine signaling 5 (SOCS5), an E3 ubiquitin ligase regulated by the transcription factor STAT5B. Interestingly, the virus-induced SOCS5 directly interacted with the anti-apoptotic B-cell lymphoma-2 (BCL2) to accelerate the BCL2 degradation through the 26S proteasome pathway. As a result, the activation of apoptosis facilitated persistent viral infection in their vector. Furthermore, STAT5B activation promoted virus amplification, whereas STAT5B suppression inhibited apoptosis and reduced virus accumulation. In summary, our results reveal that virus-induced JAK-STAT pathway regulates apoptosis to promote viral infection, and uncover a new regulatory mechanism of the JAK-STAT pathway in the persistent plant virus transmission by arthropod vectors. The Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway acts as an innate antiviral immunity in mammals, while its role in the persistent transmission of plant viruses by insect vectors remains largely unknown. In this study, we reported that plant viral infection activated the JAK-STAT pathway and this pathway regulated apoptosis to benefit virus accumulation in the insect vector. This is a new regulatory mechanism of virus-induced apoptosis for persistent viral infection. Moreover, our new findings greatly expand our knowledge on the complex crosstalk between JAK-STAT and other pathways to facilitate persistent virus transmission in their insect vectors.
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