Virus-induced drought tolerance presents a fascinating facet of biotic-abiotic interaction in plants, yet its molecular intricacies remain unclear. Our study shows that cowpea mild mottle virus (CPMMV) infection enhances drought tolerance in common bean (Phaseolus vulgaris) plants through a virus-derived small interfering RNA (vsiRNA)-activated autophagy pathway. Specifically, a 21-bp vsiRNA originating from the CPMMV Triple Gene Block1 (TGB1) gene targeted the 5' untranslated region (UTR) of the host Teosinte branched 1, Cycloidea, Proliferating Cell Factor (TCP) transcription factor gene PvTCP2, independent of the known role of TGB1 as an RNA silencing suppressor. This targeting attenuated the expression of PvTCP2, which encodes a transcriptional repressor, and in turn upregulated the core autophagy-related gene (ATG) PvATG8c, leading to activated autophagy activity surpassing the level induced by drought or CPMMV infection alone. The downstream EARLY RESPONSIVE TO DEHYDRATION (ERD) effector PvERD15 is a homologue of Arabidopsis thaliana AtERD15, which positively regulates stomatal aperture. PvERD15 was degraded in PvATG8c-mediated autophagy. Therefore, we establish a TGB1-PvTCP2-PvATG8c-PvERD15 module as a trans-kingdom fine-tuning mechanism that contributes to virus-induced drought tolerance in plant-drought-virus interactions.

中文翻译：

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病毒小干扰RNA宿主植物mRNA途径通过增强自噬调节病毒诱导的耐旱性


病毒诱导的耐旱性呈现出植物中生物-非生物相互作用的一个令人着迷的方面，但其分子复杂性仍不清楚。我们的研究表明，豇豆轻度斑驳病毒 (CPMMV) 感染通过病毒衍生的小干扰 RNA (vsiRNA) 激活的自噬途径增强菜豆 (Phaseolus vulgaris) 植物的耐旱性。具体来说，源自 CPMMV Triple Gene Block1 (TGB1) 基因的 21-bp vsiRNA 靶向宿主 Teosinte 分支 1、Cycloidea、增殖细胞因子 (TCP) 转录因子基因 PvTCP2 的 5' 非翻译区 (UTR)，独立于TGB1 作为 RNA 沉默抑制子的已知作用。这种靶向减弱了编码转录阻遏蛋白的 PvTCP2 的表达，进而上调了核心自噬相关基因 (ATG) PvATG8c，导致激活的自噬活性超过了单独由干旱或 CPMMV 感染诱导的水平。下游早期脱水响应 (ERD) 效应子 PvERD15 是拟南芥 AtERD15 的同源物，可正向调节气孔孔径。 PvERD15 在 PvATG8c 介导的自噬中被降解。因此，我们建立了 TGB1-PvTCP2-PvATG8c-PvERD15 模块作为跨界微调机制，有助于植物-干旱-病毒相互作用中病毒诱导的耐旱性。