Abstract

Initial phases of the MYMIV- Vigna mungo interaction is crucial in determining the infection phenotype upon challenging with the virus. During incompatible interaction, the plant deploys multiple stratagems that include extensive transcriptional alterations defying the virulence factors of the pathogen. Such molecular events are not frequently addressed by genomic tools. In order to obtain a critical insight to unravel how V. mungo respond to Mungbean yellow mosaic India virus (MYMIV), we have employed the PCR based suppression subtractive hybridization technique to identify genes that exhibit altered expressions. Dynamics of 345 candidate genes are illustrated that differentially expressed either in compatible or incompatible reactions and their possible biological and cellular functions are predicted. The MYMIV-induced physiological aspects of the resistant host include reactive oxygen species generation, induction of Ca2+ mediated signaling, enhanced expression of transcripts involved in phenylpropanoid and ubiquitin-proteasomal pathways; all these together confer resistance against the invader. Elicitation of genes implicated in salicylic acid (SA) pathway suggests that immune response is under the regulation of SA signaling. A significant fraction of modulated transcripts are of unknown function indicating participation of novel candidate genes in restricting this viral pathogen. Susceptibility on the other hand, as exhibited by V. mungo Cv. T9 is perhaps due to the poor execution of these transcript modulation exhibiting remarkable repression of photosynthesis related genes resulting in chlorosis of leaves followed by penalty in crop yield. Thus, the present findings revealed an insight on the molecular warfare during host-virus interaction suggesting plausible signaling mechanisms and key biochemical pathways overriding MYMIV invasion in resistant genotype of V. mungo. In addition to inflate the existing knowledge base, the genomic resources identified in this orphan crop would be useful for integrating MYMIV-tolerance trait in susceptible cultivars of V. mungo.

Highlights

  • Plant viral pathogens exhibit an obligate intracellular mode of parasitism that manipulates host resources for their own survival and proliferation [1]

  • Development of yellow mosaic pattern on leaves was intimately observed in susceptible plants that started with the appearance of bright yellow specks coalescing into larger lesions

  • V. mungo plants were fully symptomatic at 15 dpi, visual symptoms started appearing from 5–7 dpi in the compatible host while establishment of pathogen was severely impaired in resistant VMR84 (Fig 2A)

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Summary

Introduction

Plant viral pathogens exhibit an obligate intracellular mode of parasitism that manipulates host resources for their own survival and proliferation [1]. Due to their limited genetic capability, these pathogens entirely depend on the host’s machinery to complete their life cycle. In doing so, they utilize diverse stratagems to conquer the host, upsetting hosts immune response by escaping its surveillance [2, 3]. Disease manifestation is an organized consequence of pathogen establishment and emergence of disease symptoms in the compatible host. A cascade of signaling events are elicited that culminates with the formulation of appropriate responses enabling the host to defend against the potential invader

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