北京大学李毅课题组PLoS Pathogen揭示病毒侵染新机制

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2016年9月8日，国际微生物学知名期刊《PLOS Pathogens》在线发表了北京大学生命科学学院李毅研究组题为“Rice Dwarf Virus P2 Protein Hijacks Auxin Signaling by Directly Targeting the Rice OsIAA10 Protein, Enhancing Viral Infection and Disease Development”的研究论文，论文报道了病毒蛋白通过调控生长素信号通路帮助病毒侵染的一种新机制 。生命学院博士后晋莲为论文第一作者，李毅教授为论文通讯作者。


生长素通路在植物的生长发育中发挥重要的功能，然而人们对生长素通路和病原菌侵染的关系并不清楚。水稻矮缩病毒（Rice dwarf phytoreovirus，RDV）是由叶蝉传播的能够引起大面积水稻感病并严重减产的一种病毒。RDV侵染后的水稻矮化，分蘖增多，冠根变短症状和生长素通路一些突变体表型很像。

李毅研究组用生长素处理健康和RDV感染的水稻，发现RDV感染造成水稻的生长素响应受阻，对生长素的敏感度降低。研究组通过酵母双杂筛库，发现RDV的外壳蛋白P2与水稻中生长素通路抑制子兼共受体Aux/IAA家族蛋白OsIAA10相互作用。通过进一步的研究，研究组发现P2是通过和OsIAA10的Domain II相互作用，进而影响了OsIAA10和OsTIR1的结合，从而抑制OsIAA10通过26S酶体途径的降解，使得感病水稻中OsIAA10的蛋白积累量比健康水稻中的显著增高。另外，过量表达OsIAA10或者其不能被降解突变体蛋白OsIAA10P116L表型同RDV感病水稻相似，并且对RDV侵染的更敏感；而通过RNAi的方式降低OsIAA10的表达能够提高水稻对RDV的抗性。这表明P2和OsIAA10互作引起的OsIAA10蛋白的稳定和积累量增多而导致生长素通路响应的受阻是RDV症状形成的诱因之一，而且有利于RDV的复制侵染。该研究揭示了一个病毒蛋白通过干扰OsIAA10的降解、破坏生长素信号通路来帮助病毒侵染和复制的新机制。

RDV调控水稻中生长素信号通路的模式图

该研究已于2016年9月8日以标题“Rice Dwarf Virus P2 Protein Hijacks Auxin Signaling by Directly Targeting the Rice OsIAA10 Protein，Enhancing Viral Infection and Disease Development”在PLoS Pathogens在线发表。李毅教授为该文的通讯作者。生命学院博士后晋莲为该文的第一作者。该研究得到了国家自然科学基金、科技部国家重点基础研究发展计划（973计划）和国家转基因专项的资助。

[size=0.8465em]PLoS Pathog. 2016 Sep 8;12(9):e1005847. doi: 10.1371/journal.ppat.1005847. eCollection 2016.

Rice Dwarf Virus P2 Protein Hijacks Auxin Signaling by Directly Targeting the Rice OsIAA10 Protein, EnhancingViral Infection and Disease Development.[size=0.923em]Jin L[size=0.8461em]1, Qin Q[size=0.8461em]1, Wang Y[size=0.8461em]1, Pu Y[size=0.8461em]1, Liu L[size=0.8461em]1, Wen X[size=0.8461em]1, Ji S[size=0.8461em]1, Wu J[size=0.8461em]1, Wei C[size=0.8461em]1, Ding B[size=0.8461em]2, Li Y[size=0.8461em]1.



Abstract

The phytohormone auxin plays critical roles in regulating myriads of plant growth and developmental processes. Microbe infection can disturbauxin signaling resulting in defects in these processes, but the underlying mechanisms are poorly understood. Auxin signaling begins with perception of auxin by a transient co-receptor complex consisting of an F-box transport inhibitor response 1/auxin signaling F-box (TIR1/AFB)protein and an auxin/indole-3-acetic acid (Aux/IAA) protein. Auxin binding to the co-receptor triggers ubiquitination and 26S proteasome degradation of the Aux/IAA proteins, leading to subsequent events, including expression of auxin-responsive genes. Here we report that Rice dwarfvirus (RDV), a devastating pathogen of rice, causes disease symptoms including dwarfing, increased tiller number and short crown roots in infected rice as a result of reduced sensitivity to auxin signaling. The RDV capsid protein P2 binds OsIAA10, blocking the interaction betweenOsIAA10 and OsTIR1 and inhibiting 26S proteasome-mediated OsIAA10 degradation. Transgenic rice plants overexpressing wild-type or a dominant-negative (degradation-resistant) mutant of OsIAA10 phenocopy RDV symptoms are more susceptible to RDV infection; however, knockdown of OsIAA10 enhances the resistance of rice to RDV infection. Our findings reveal a previously unknown mechanism of viral proteinreprogramming of a key step in auxin signaling initiation that enhances viral infection and pathogenesis.

来源：北京大学，pubmed