A viral small interfering RNA-host plant mRNA pathway modulates virus-induced drought tolerance by enhancing autophagy.

IF 10 1区生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Plant Cell Pub Date : 2024-09-03 DOI:10.1093/plcell/koae158

Xinyang Wu, Shuting Chen, Zixin Zhang, Weixin Zhou, Ting Sun, Kang Ning, Min Xu, Xubo Ke, Pei Xu

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引用次数: 0

Abstract

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 nt 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.

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病毒小干扰 RNA-寄主植物 mRNA 通路通过增强自噬调节病毒诱导的耐旱性。

病毒诱导的耐旱性是植物中生物-生物相互作用的一个迷人方面，但其分子的复杂性仍不清楚。我们的研究表明，豇豆轻度斑驳病毒（CPMMV）感染可通过病毒衍生的小干扰 RNA（vsiRNA）激活的自噬途径增强蚕豆（Phaseolus vulgaris）植株的耐旱性。具体来说，源自 CPMMV 三重基因阻断1（TGB1）基因的 21-bp vsiRNA 靶向宿主 Teosinte branched 1, Cycloidea, Proliferating Cell Factor (TCP) 转录因子基因 PvTCP2 的 5' 非翻译区 (UTR)，而非已知的 TGB1 作为 RNA 沉默抑制因子的作用。这种靶向作用削弱了编码转录抑制因子的 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干旱或 CPMMV 感染单独诱导的水平。下游的早期脱氢反应（ERD）效应因子 PvERD15 是拟南芥 AtERD15 的同源物，它对气孔开度有正向调节作用。PvERD15 在 PvATG8c 介导的自噬过程中被降解。因此，我们建立了一个 TGB1-PvTCP2-PvATG8c-PvERD15 模块，作为植物-干旱-病毒相互作用中有助于病毒诱导的耐旱性的跨领域微调机制。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Plant Cell 生物-生化与分子生物学

CiteScore

16.90

自引率

5.20%

发文量

337

审稿时长

2.4 months

期刊介绍： Title: Plant Cell Publisher: Published monthly by the American Society of Plant Biologists (ASPB) Produced by Sheridan Journal Services, Waterbury, VT History and Impact: Established in 1989 Within three years of publication, ranked first in impact among journals in plant sciences Maintains high standard of excellence Scope: Publishes novel research of special significance in plant biology Focus areas include cellular biology, molecular biology, biochemistry, genetics, development, and evolution Primary criteria: articles provide new insight of broad interest to plant biologists and are suitable for a wide audience Tenets: Publish the most exciting, cutting-edge research in plant cellular and molecular biology Provide rapid turnaround time for reviewing and publishing research papers Ensure highest quality reproduction of data Feature interactive format for commentaries, opinion pieces, and exchange of information in review articles, meeting reports, and insightful overviews.

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