Abstract

Key MessageDynamic transcriptome profiling revealed excessive, yet ineffective, immune response toV. nonalfalfaeinfection in susceptible hop, global gene downregulation in shoots of resistant hop and only a few infection-associated genes in roots.Hop (Humulus lupulus L.) production is hampered by Verticillium wilt, a disease predominantly caused by the soil-borne fungus Verticillium nonalfalfae. Only a few hop cultivars exhibit resistance towards it and mechanisms of this resistance have not been discovered. In this study, we compared global transcriptional responses in roots and shoots of resistant and susceptible hop plants infected by a lethal strain of V. nonalfalfae. Time-series differential gene expression profiles between infected and mock inoculated plants were determined and subjected to network-based analysis of functional enrichment. In the resistant hop cultivar, a remarkably low number of genes were differentially expressed in roots in response to V. nonalfalfae infection, while the majority of differentially expressed genes were down-regulated in shoots. The most significantly affected genes were related to cutin biosynthesis, cell wall biogenesis, lateral root development and terpenoid biosynthesis. On the other hand, susceptible hop exhibited a strong defence response in shoots and roots, including increased expression of genes associated with plant responses, such as innate immunity, wounding, jasmonic acid pathway and chitinase activity. Strong induction of defence-associated genes in susceptible hop and a low number of infection-responsive genes in the roots of resistant hop are consistent with previous findings, confirming the pattern of excessive response of the susceptible cultivar, which ultimately fails to protect the plant from V. nonalfalfae. This research offers a multifaceted overview of transcriptional responses of susceptible and resistant hop cultivars to V. nonalfalfae infection and represents a valuable resource in the study of this plant-pathogen interaction.

Highlights

  • Key Message Dynamic transcriptome profiling revealed excessive, yet ineffective, immune response to V. nonalfalfae infection in susceptible hop, global gene downregulation in shoots of resistant hop and only a few infection-associated genes in roots

  • Hop (Humulus lupulus L.) production is hampered by Verticillium wilt, a disease predominantly caused by the soil-borne fungus Verticillium nonalfalfae

  • At the early stages of infection by vascular plant pathogens, plant defence relies on protective physical barriers (e.g., Casparian strips, suberin), preformed chemical defence compounds and general immune responses induced by microbe-associated molecular patterns (MAMPs) (De Coninck et al 2014)

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Summary

Introduction

Key Message Dynamic transcriptome profiling revealed excessive, yet ineffective, immune response to V. nonalfalfae infection in susceptible hop, global gene downregulation in shoots of resistant hop and only a few infection-associated genes in roots. Once the pathogens reach the xylem vessels, they are presumably recognized by specific extracellular receptors in the surrounding parenchyma cells This recognition activates the formation of tyloses, the accumulation of pectin-rich gels and gums, vascular coating and callose and secondary cell wall depositions (Yadeta and Thomma 2013; De Coninck et al 2014; Cregeen et al 2015). Plant microarray and RNA-Seq studies have revealed that the interaction between vascular wilt pathogens and host plants involves transcriptional reprogramming of hundreds of genes, activation of Ca2?-signalling pathways, induction of ROS and MAPK cascades and modulation of phytohormone signalling (Hu et al 2008; van Esse et al 2009; Chen et al 2014). Global transcriptome profiling and DEGs analysis were carried out on sunflower—V. dahliae interactions, revealing massive transcriptional reprogramming and classifying resistant cultivar DEGs into plant hormone signalling transduction, plant-pathogen interaction and flavonoid biosynthesis functional categories (Guo et al 2017)

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