https://mp.weixin.qq.com/s/zmoxBy67OkV3SG2YI2LYLA

原創(chuàng) 吳昕揚(yáng) 植物脅迫與抗逆研究

近日，福建農(nóng)林吳建國(guó)教授團(tuán)隊(duì)在JIPB發(fā)表了題為《An AGO2–miR167g-3p–SNAP32 module confers antiviral immunity in rice》的研究論文，揭示了AGO2–miR167g-3p–SNAP32模塊介導(dǎo)水稻抗病毒免疫。

AGO蛋白是RNA沉默通路的核心，并在植物抗病毒防御中發(fā)揮關(guān)鍵作用。然而，水稻中單個(gè)AGO的功能仍不完全明晰。

本研究證明，水稻AGO2通過(guò)涉及miR167g-3p及其靶基因SNAP32的調(diào)控模塊，有助于增強(qiáng)對(duì)水稻鋸齒葉矮縮病毒（RRSV）的抗性。

免疫沉淀結(jié)合小RNA測(cè)序顯示，AGO2不僅與病毒衍生的小干擾RNA（vsiRNA）結(jié)合，還優(yōu)先與miR167g-3p結(jié)合，尤其是在RRSV感染期間。

功能分析進(jìn)一步表明，RRSV感染時(shí)誘導(dǎo)miR167g-3p表達(dá)。轉(zhuǎn)基因稻株過(guò)表達(dá)miR167g-3p表現(xiàn)出抗性增強(qiáng)，而敲低系則更易感。通過(guò)在煙草的瞬時(shí)表達(dá)測(cè)定和水稻原質(zhì)體中的雙熒光素酶測(cè)定，證明SNAP32是miR167g-3p的直接靶基因。表達(dá)分析也證實(shí)miR167g-3p在轉(zhuǎn)錄本層面抑制SNAP32。

相應(yīng)地，SNAP32過(guò)表達(dá)的植株對(duì)RRSV的易感性增加，而snap32基因敲除植株的抗性增強(qiáng)，支持SNAP32在抗病毒防御中的負(fù)調(diào)控作用。

綜合這些發(fā)現(xiàn)，作者建立了一條調(diào)控通路，AGO2通過(guò)穩(wěn)定miR167g-3p抑制SNAP32，從而限制RRSV感染，從而促進(jìn)抗病毒免疫。這項(xiàng)工作推動(dòng)了人們對(duì)水稻AGO2介導(dǎo)防御的理解，并揭示AGO-miRNA-靶標(biāo)復(fù)合體中miRNA 3p鏈可作為抗病毒防御的新機(jī)制，為植物抵御病毒病原體提供了重要見(jiàn)解。

Argonaute proteins (AGOs) are central to RNA silencing pathways and play critical roles in plant antiviral defense. However, the functions of individual AGOs in rice remain incompletely understood. In this study, we demonstrate that rice AGO2 contributes to resistance against rice ragged stunt virus (RRSV) through a regulatory module involving miR167g-3p and its target gene, SNAP32. Immunoprecipitation coupled with small RNA sequencing revealed that AGO2 associates not only with virus-derived small interfering RNAs (vsiRNAs) but also preferentially associates with miR167g-3p during RRSV infection. Functional analyses further showed that miR167g-3p expression is induced upon infection. Transgenic rice lines overexpressing miR167g-3p exhibited enhanced resistance, whereas knockdown lines were more susceptible. SNAP32 was validated as a direct target of miR167g-3p through transient expression assays in Nicotiana benthamiana and dual-luciferase assays in rice protoplasts. Expression analyses confirmed that miR167g-3p represses SNAP32 at the transcript level. Consistently, SNAP32-overexpressing plants displayed increased susceptibility to RRSV, while snap32knockout plants showed enhanced resistance, supporting a negative role of SNAP32 in antiviral defense. Together, these findings establish a regulatory pathway in which AGO2 promotes antiviral immunity by stabilizing miR167g-3p to repress SNAP32, thereby restricting RRSV infection. This work advances our understanding of AGO2-mediated defense in rice and highlights the use of a miRNA 3p strand within an AGO–miRNA-target module as an important layer of resistance against viral pathogens.