RNAi-Based Antiviral Innate Immunity in Plants.

Liying Jin,Zhongxin Guo,Meiqin Xiang,Mengna Chen

doi:10.3390/v14020432

Liying Jin, Zhongxin Guo + Show 2 more

Open Access

https://doi.org/10.3390/v14020432

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Journal: Viruses	Publication Date: Feb 20, 2022
Citations: 20	License type: CC BY 4.0

Affiliation: Fujian Agriculture and Forestry University

Abstract

Multiple antiviral immunities were developed to defend against viral infection in hosts. RNA interference (RNAi)-based antiviral innate immunity is evolutionarily conserved in eukaryotes and plays a vital role against all types of viruses. During the arms race between the host and virus, many viruses evolve viral suppressors of RNA silencing (VSRs) to inhibit antiviral innate immunity. Here, we reviewed the mechanism at different stages in RNAi-based antiviral innate immunity in plants and the counteractions of various VSRs, mainly upon infection of RNA viruses in model plant Arabidopsis. Some critical challenges in the field were also proposed, and we think that further elucidating conserved antiviral innate immunity may convey a broad spectrum of antiviral strategies to prevent viral diseases in the future.

Highlights

The phenomenon of RNA silencing was first observed in plants in 1990 when the introduction of chalcone synthase transgene into petunia led to the suppression of endogenous homological genes [1,2]
In 1998, Andrew Fire and Craig Mello found that double-stranded RNAs caused potent and specific interference in Caenothabditis elegan [3] and termed the phenomenon RNA interference (RNAi), which won the Nobel Prize in Physiology and Medicine in 2006 and opened up a revolution in the field of biology [3,4]
Numerous studies showed that RNAi was evolutionarily conserved in eukaryotes, and it regulated all aspects of biological events [5,6]

Summary

Introduction

The phenomenon of RNA silencing was first observed in plants in 1990 when the introduction of chalcone synthase transgene into petunia led to the suppression of endogenous homological genes [1,2]. MiRNAs and siRNA are, respectively, produced from the processing of hair-pin RNA or dsRNA by a specific Dicer. DCL3 generates 24nt siRNAs to regulate RNA-dependent DNA methylation (RdDM) in transcriptional gene silencing (TGS) in Arabidopsis [41]. In RNAi-based antiviral innate immunity, DCL4 perceives and cuts long viral dsRNA to produce 21 nt vsiRNA to prevent viral infection, especially after the infection of RNA virus in Arabidopsis and other plants [49]. Each DCL is responsible for the production of distinct small RNA, they may function redundantly or hierarchically in RNAi-based antiviral innate immunity. DRB4 interacts with DCL4 to form another kind of dicing body for the efficient processing of siRNAs. It was reported that the DRB4 mutation resulted in defective antiviral defense to the infection of turnip yellow mosaic virus (TYMV) [67]. DRB2 was recently characterized as a wide-spectrum antiviral effector; overexpression of DRB2 decreased the accumulation of several different RNA viruses, including tobacco rattle virus (TRV), tomato bushy stunt virus (TBSV), potato virus X (PVX), and grapevine fanleaf virus (GFLV) [68]

Production and Amplification of vsiRNA

Viral Suppressors of RNAi

Question and Perspective