J Integr Plant Biol ›› 2026, Vol. 68 ›› Issue (5): 1523-1541.DOI: 10.1111/jipb.70166

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  • 收稿日期:2025-10-06 接受日期:2026-01-06 出版日期:2026-05-01 发布日期:2026-05-08

Insect infestation-induced autophagic degradation of OsPR1a fine-tunes rice salicylic acid defenses to benefit vector-borne virus transmission

Jingya Zhao, Hongxiang Zhang, Yupeng Tang, Chunyu Zhang, Yuting Chen, Dongsheng Jia, Hongyan Chen and Taiyun Wei*   

  1. State Key Laboratory of Agriculture and Forestry Biosecurity, Vector‐borne Virus Research Center, Fujian Province Key Laboratory of Plant Virology, Institute of Plant Virology, Fujian Agriculture and Forestry University, Fuzhou 350002, Fujian, China†These authors contributed equally to this article.*Correspondence: Taiyun Wei (weitaiyun@fafu.edu.cn)
  • Received:2025-10-06 Accepted:2026-01-06 Online:2026-05-01 Published:2026-05-08
  • Supported by:
    This work was supported by the National Key Research andDevelopment Program of China (2023YFD1400300) and theNational Natural Science Foundation of China (32202270).

Abstract: While plant salicylic acid (SA) signaling via NPR1-PR1 is well-characterized in pathogen resistance, its role against piercing-sucking insects remains unclear in rice. Here, we demonstrate that leafhopper infestation in rice induces SA-mediated resistance, which defends against insect infestation via pathogenesis-related protein OsPR1a. However, prolonged infestation triggers autophagy-dependent degradation of OsPR1a through its interaction with OsATG8b, fine-tuning immunity to prevent excessive defense activation. Strikingly, this autophagy-mediated OsPR1a degradation represents a conserved regulatory mechanism in rice during brown planthopper infestation. A rice rhabdovirus in leafhopper vectors secretes glycoprotein on virion envelopes to rice phloem, where it binds OsATG6b and OsPR1a to enhance autophagic OsPR1a turnover, ultimately facilitating insect vector feeding and viral transmission by leafhopper vectors. Our work reveals an adaptive mechanism by which a vector-borne virus hijacks plant autophagy to evade SA immunity, highlighting OsPR1a as a critical convergence point in plant-insect-virus interactions.

Key words: autophagy, OsPR1a, plant-insect-virus interactions, salicylic acid, virus transmission

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