Barley stripe mosaic virus infection requires PKA-mediated phosphorylation of γb for suppression of both RNA silencing and the host cell death response
Barley stripe mosaic virus infection requires PKA-mediated phosphorylation of γb for suppression of both RNA silencing and the host cell death response
复制标题
大麦条纹花叶病毒感染需要 PKA 介导的 β 磷酸化来抑制 RNA 沉默和宿主细胞死亡反应
DOI:
10.1111/nph.15065
复制
发表时间:
2018
期刊:
影响因子:
9.4
通讯作者:
Li Dawei
中科院分区:
文献类型:
--
作者:
Zhang Xuan;Dong Kai;Xu Kai;Zhang Kun;Jin Xuejiao;Yang Meng;Zhang Yongliang;Wang Xianbing;Han Chenggui;Yu Jialin;Li Dawei
TheBarley stripe mosaic virus(BSMV) γb protein is a viral suppressor of RNA silencing (VSR) and symptom determinant. However, it is unclear how post‐translational modification affects the different functions of γb.Here, we demonstrate that γb is phosphorylated at Ser‐96 by a PKA‐like kinasein vivoandin vitro. Mutant viruses containing a nonphosphorylatable substitution (BSMVS96Aor BSMVS96R) exhibited reduced viral accumulation inNicotiana benthamianadue to transient induction of the cell death response that constrained the virus to necrotic areas. By contrast, a BSMVS96Dmutant virus that mimics γb phosphorylation spread similarly to the wild‐type virus.Furthermore, the S96A mutant had reduced local and systemic γb VSR activity due to having compromised its binding activity to 21‐bp dsRNA. However, overexpression of other VSRsin transorin cisfailed to rescue the necrosis induced by BSMVS96A, demonstrating that suppression of cell death by γb phosphorylation is functionally distinct from its RNA silencing suppressor activities.These results provide new insights into the function of γb phosphorylation in regulating RNA silencing and the BSMV‐induced host cell death response, and contribute to our understanding of how the virus optimizes the balance between viral replication and virus survival in the host plants during virus infection.