Ramesh S V, Yogindran Sneha, Gnanasekaran Prabu, Chakraborty Supriya, Winter Stephan, Pappu Hanu R
ICAR-Central Plantation Crops Research Institute, Kasaragod, India.
School of Life Sciences, Jawaharlal Nehru University, New Delhi, India.
Front Microbiol. 2021 Jan 14;11:614231. doi: 10.3389/fmicb.2020.614231. eCollection 2020.
Virus-derived siRNAs (vsiRNAs) generated by the host RNA silencing mechanism are effectors of plant's defense response and act by targeting the viral RNA and DNA in post-transcriptional gene silencing (PTGS) and transcriptional gene silencing (TGS) pathways, respectively. Contrarily, viral suppressors of RNA silencing (VSRs) compromise the host RNA silencing pathways and also cause disease-associated symptoms. In this backdrop, reports describing the modulation of plant gene(s) expression by vsiRNAs via sequence complementarity between viral small RNAs (sRNAs) and host mRNAs have emerged. In some cases, silencing of host mRNAs by vsiRNAs has been implicated to cause characteristic symptoms of the viral diseases. Similarly, viroid infection results in generation of sRNAs, originating from viroid genomic RNAs, that potentially target host mRNAs causing typical disease-associated symptoms. Pathogen-derived sRNAs have been demonstrated to have the propensity to target wide range of genes including host defense-related genes, genes involved in flowering and reproductive pathways. Recent evidence indicates that vsiRNAs inhibit host RNA silencing to promote viral infection by acting as decoy sRNAs. Nevertheless, it remains unclear if the silencing of host transcripts by viral genome-derived sRNAs are inadvertent effects due to fortuitous pairing between vsiRNA and host mRNA or the result of genuine counter-defense strategy employed by viruses to enhance its survival inside the plant cell. In this review, we analyze the instances of such cross reaction between pathogen-derived vsiRNAs and host mRNAs and discuss the molecular insights regarding the process of pathogenesis.
宿主RNA沉默机制产生的病毒衍生小干扰RNA(vsiRNA)是植物防御反应的效应因子,分别通过在转录后基因沉默(PTGS)和转录基因沉默(TGS)途径中靶向病毒RNA和DNA来发挥作用。相反,RNA沉默的病毒抑制因子(VSR)会损害宿主RNA沉默途径,并引发与疾病相关的症状。在此背景下,出现了一些报告,描述了vsiRNA通过病毒小RNA(sRNA)与宿主mRNA之间的序列互补性对植物基因表达的调控。在某些情况下,vsiRNA对宿主mRNA的沉默被认为会导致病毒疾病的特征性症状。同样,类病毒感染会导致源自类病毒基因组RNA的sRNA产生,这些sRNA可能靶向宿主mRNA,引发典型的与疾病相关的症状。病原体衍生的sRNA已被证明有靶向广泛基因的倾向,包括宿主防御相关基因、参与开花和生殖途径的基因。最近的证据表明,vsiRNA通过充当诱饵sRNA来抑制宿主RNA沉默,从而促进病毒感染。然而,病毒基因组衍生的sRNA对宿主转录本的沉默是由于vsiRNA与宿主mRNA之间偶然配对产生的意外效应,还是病毒为增强其在植物细胞内的生存而采用的真正反防御策略的结果,仍不清楚。在这篇综述中,我们分析了病原体衍生的vsiRNA与宿主mRNA之间这种交叉反应的实例,并讨论了关于发病机制过程的分子见解。