Antiviral RNAi mediated Plant defense versus its suppression by viruses

The age-old battle between plants and viruses has many twists and turns. Plants acquired the RNAi factors to checkmate the viruses and the viruses encode VSRs to defeat RNAi for their own survival. Plants designed mechanisms to neutralize the toxic effects of VSRs and the viruses, in their turn, use host microRNAs to strengthen their infection processes. The infi ghtings between these two entities will take different shapes with prolonged evolution and accordingly the researchers will dig these novel forms of duels not only to throw lights in the involved mechanisms but also to manipulate various antiviral strategies. Some of the research courses that might come up in the immediate future are discussed. Commentary Antiviral RNAi mediated Plant defense versus its suppression by viruses Dinesh Gupta1 and Sunil Kumar Mukherjee2* 1Translational Bioinformatics Group, ICGEB, New Delhi, India 2Division of Plant Pathology, IARI, New Delhi, India *Address for Correspondence: Sunil Kumar Mukherjee, Division of Plant Pathology, IARI, New Delhi, India, Tel: +91-9871995629; 011-2584-3588; Fax: 011-2584-0772; Email: sunilmukherjeeudsc@gmail.com Submitted: 27 December 2018 Approved: 24 January 2019 Published: 25 January 2019 Copyright: © 2019 Gupta D, et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited How to cite this article: Gupta D, Mukherjee SK. Antiviral RNAi mediated Plant defense versus its suppression by viruses. J Plant Sci Phytopathol. 2019; 3: 001-008. https://doi.org/10.29328/journal.jpsp.1001025 The arms race between host and virus is a continually evolving process involving multiple layers of interactions. Most of all eukaryotic organisms are RNAi-competent and defend themselves against the intruding molecular parasites, namely Viruses and Transposons [1]. As a reaction to host-defense (or rather counterdefence), viruses have also generated multiple weapons in their armory. The hosts in turn tighten up their security by developing means of counter-counterdefence. Viruses also reciprocate and invent strategies to weaken the hosts in subsequent rounds. All plant viruses encode RNAi-suppressors (VSRs) and use them to battle the host RNA-factors to uphold their counter-defense [2]. The VSRs are deactivated by hosts by mechanisms known as counter-counter defense. Following viral invasion in plants, host-microRNA (miR) pro iles undergo a lot of changes [3]. A subset of these deregulated miRs likely works against viral invasion, multiplication and systemic propagation [4,5]. However, recent reports indicate that some of the virus-induced miRs are also used to sensitise the host for enhancing viral invasion. Of the latter category, we would like to choose only three miRs, namely miR168, miR6026 and miR319 here as the representative candidates for their ability to sustain viral growth. There are other miRs who also work in similar pathway but we have chosen the above three because of the preponderance of literature reports. Following entry of viruses in the plant cell, ds-RNA intermediates of viral genomes; viral transcripts etc. are generated due to various reasons like viral genome replication/ transcription, convergent transcriptions from viral genomes or hosts’ RNA dependent RNA Polymerases activities on the viral transcripts etc. These dsRNAs are diced by DCLs to produce small RNAs which are known as V-siRNAs [6]. The V-siRNAs are further ampli ied by host-dependent processes and are known as secondary V-siRNAs or Va-siRNAs [7]. These V-siRNAs, along with Va-siRNAs, either slice or translationally inhibit the viral mRNAs in RISC mediated processes and eventually reduce the virus titer [8]. Various host factors work in this host-defense pathway and are known as antiviral RNAi factors. The core defense factors include RDRs (mostly RDR6, RDR2, RDR1), DCLs (mostly DCL4, followed by DCL2), and AGO proteins (AGO1, AGO2, AGO3, AGO4, Antiviral RNAi mediated Plant defense versus its suppression by viruses Published: January 25, 2019 002 AGO5, AGO7, AGO10 etc.). A list of these factors in arabidopsis and rice are shown in table 1. Generally, DCL4 is the major producer of V-siRNA with DCL2 playing the second iddle. However, there are few instances where DCL2 plays the major role over DCL4, for example, the patho-system of Tomato Mosaic Virus (ToMV) and tomato [9]. DCL3 also participates in case of viruses with single-stranded DNA genomes, namely begomoviruses, to transcriptionally silence the viral DNA genome [10]. The v-siRNAs of three different sizes (21/22/24 bps) spread from the source of production to distant non-infected cells in systemic fashions and thus protect the distant cells against incoming viral invasion. This systemic activity is facilitated by DCL2 while DCL4 plays the antagonistic inhibitory role [11,12]. In addition to the core factors, a few other accessory antiviral factors have recently been screened genetically and are listed in table 2 [13,14]. Besides the V-siRNAs, the deregulated host miRs caused by viral invasions also play antiviral roles [5]. A set of plant miRs have been bioinformatically postulated that retain the ability to silence viral ORFs, and only a couple of them have been validated experimentally [4]. Plum pox virus (PPV) chimeras harbor plant miRNA target sequences and these are functional in Arabidopsis, and were also silenced by miRNA function in three different host plants [15]. Some tomato miRs are also known to produce phasiRNAs with antiviral activity [9]. The generations of the 21-nuclotide phasiRNAs are initiated by the action of DCL2-made 22-mer miRs on several diseaserelated genes; and factors like DCL4, together with AGO1, AGO4, AGO7, SUPPRESSOR OF GENE SILENCING3 (SGS3), RDR6, and DOUBLE-STRANDED RNA BINDING FACTOR 4 (DRB4) etc. are involved in different steps of phasiRNA synthesis [16]. Viruses have also evolved to defeat the antiviral RNAi pathways, mostly by encoding proteins from their genomes that are known as RNAi suppressors. These suppressors not only counteract host defense but also participate in other pathways necessary for the viral life cycle. These are very important for viral replication and Table 1: Core antiviral RNAi factors.