Abstract

Grapevine downy mildew (DM) is a destructive oomycete disease of viticulture worldwide. MrRPV1 is a typical TIR-NBS-LRR type DM disease resistance gene cloned from the wild North American grapevine species Muscadinia rotundifolia. However, the molecular basis of resistance mediated by MrRPV1 remains poorly understood. Downy mildew-susceptible Vitis vinifera cv. Shiraz was transformed with a genomic fragment containing MrRPV1 to produce DM-resistant transgenic Shiraz lines. Comparative transcriptome analysis was used to compare the transcriptome profiles of the resistant and susceptible genotypes after DM infection. Transcriptome modulation during the response to P. viticola infection was more rapid, and more genes were induced in MrRPV1-transgenic Shiraz than in wild-type plants. In DM-infected MrRPV1-transgenic plants, activation of genes associated with Ca2+ release and ROS production was the earliest transcriptional response. Functional analysis of differentially expressed genes revealed that key genes related to multiple phytohormone signaling pathways and secondary metabolism were highly induced during infection. Coexpression network and motif enrichment analysis showed that WRKY and MYB transcription factors strongly coexpress with stilbene synthase (VvSTS) genes during defense against P. viticola in MrRPV1-transgenic plants. Taken together, these findings indicate that multiple pathways play important roles in MrRPV1-mediated resistance to downy mildew.

Highlights

  • Plants have evolved complex and sophisticated defense mechanisms to cope with the threat of pests and diseases

  • In this study, we utilized transgenic Shiraz plants carrying the MrRPV1 resistance gene from M. rotundifolia to investigate the mechanism by which this gene confers resistance to downy mildew (DM)

  • Significantly fewer differentially expressed genes (DEGs) were identified using this approach than using comparisons of transcription profiles of DM-susceptible and DMresistant grapevines with very different genetic backgrounds[20,21,22,25]

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Summary

Introduction

Plants have evolved complex and sophisticated defense mechanisms to cope with the threat of pests and diseases. These defense mechanisms can be divided into two layers of immune responses, PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI)[1]. PTI is the first layer of immune defense and is triggered the detection of conserved microbe- or pathogen-associated molecular patterns (MAMPs/PAMPs) or self-molecules (damage-associated molecular patterns, DAMPs) by pattern-recognition terminal domain shares homology with cytosolic domains of Drosophila Toll or animal interleukin-1 receptors (TIR-NBS-LRR) or has a predicted coiled-coil domain (CC-NBS-LRR)[4]. Grapevine downy mildew (DM), caused by the oomycete Plasmopara viticola[5,6], is a serious disease of viticulture worldwide.

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