Authors
Han-Wei Li, Jin-Ying Wang, Can Liu, Yin-Shuai Xie, Shang-Zhen Yu, Chen-Lu Feng, Wen-Hao Zhang, Meng-Qi Ma, Yi-Xuan Wang, Tian-Zhong Li, Yu-Qin Cheng
Published in
Plant physiology. Jul 22, 2026. Epub Jul 22, 2026.
Abstract
Grapevine (Vitis vinifera) is severely impacted by viral diseases, with grapevine leafroll disease (GLRD) being the most economically damaging. Grapevine leafroll-associated virus 2 (GLRaV-2) is a prevalent virus associated with GLRD, yet the molecular mechanisms underlying GLRaV-2 infection remain poorly understood. Here, we demonstrate that the grapevine transcription factor (TF) VvWRKY51 positively autoregulates its transcription and directly represses salicylic acid (SA)-responsive defense genes VvPR1 (pathogenesis-related gene 1), VvPR2, and VvPR5. Through in vivo and in vitro assays, we demonstrate that GLRaV-2 RNA silencing suppressor p24 specifically interacts with VvWRKY51 to promote viral infection. p24 hijacks nuclear VvWRKY51 by translocating it to the cytoplasm, thereby enhancing its RNA silencing suppression activity via two mechanisms: (a) evading host degradation pathways (ubiquitin-proteasome system and autophagy), and (b) strengthening its siRNA-binding affinity. Concurrently, cytoplasmic p24 enters the nucleus by binding VvWRKY51, where it reinforces VvWRKY51-mediated transcriptional repression of VvPR1, VvPR2, and VvPR5. This occurs by enhancing VvWRKY51 binding to its own promoter and those of VvPR genes. Our findings reveal a novel viral strategy wherein a single viral suppressor of RNA silencing (VSR) simultaneously suppresses RNA silencing and SA-mediated immunity by interacting with a host TF to establish a permissive environment for infection.
PMID:
42485612
Bibliographic data and abstract were imported from PubMed on 23 Jul 2026.
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