Genetic and transcriptional dissection of resistance to Claviceps purpurea in the durum wheat cultivar Greenshank

Anna Gordon,Ron E Knox,Vijai Bhadauria,Lesley A Boyd,Caroline Hadley,Donal M O’Sullivan,Ya-Chih Hsueh,Nelzo Ereful,Jim G Menzies,Curt Mccartney,David J Konkin,Mara Sgroi,Colin W Hiebert

doi:10.1007/s00122-020-03561-9

Abstract

Key messageFour QTL for ergot resistance (causal pathogen Claviceps purpurea) have been identified in the durum wheat cultivar Greenshank.Claviceps purpurea is a pathogen of grasses that infects flowers, replacing the seed with an ergot sclerotium. Ergot presents a significant problem to rye, barley and wheat, in particular hybrid seed production systems. In addition, there is evidence that the highly toxic alkaloids that accumulate within sclerotia can cross-contaminate otherwise healthy grain. Host resistance to C. purpurea is rare, few resistance loci having been identified. In this study, four ergot resistance loci are located on chromosomes 1B, 2A, 5A and 5B in the durum wheat cv. Greenshank. Ergot resistance was assessed through analysis of phenotypes associated with C. purpurea infection, namely the number of inoculated flowers that produced sclerotia, or resulted in ovary death but no sclerotia, the levels of honeydew produced, total sclerotia weight and average sclerotia weight and size per spike. Ergot testing was undertaken in Canada and the UK. A major effect QTL, QCp.aafc.DH-2A, was detected in both the Canadian and UK experiments and had a significant effect on honeydew production levels. QCp.aafc.DH-5B had the biggest influence on total sclerotia weight per spike. QCp.aafc.DH-1B was only detected in the Canadian experiments and QCp.aafc.DH-5A in the UK experiment. An RNASeq analysis, undertaken to identify wheat differentially expressed genes associated with different combinations of the four ergot resistance QTL, revealed a disproportionate number of DEGs locating to the QCp.aafc.DH-1B, QCp.aafc.DH-2A and QCp.aafc.DH-5B QTL intervals.

Highlights

Ergot, caused by the fungal pathogen Claviceps purpurea (Fr.) Tul. (Cp), is a disease of cereals and grasses that infects female flowers at anthesis (Fig. 1; Menzies and Turkington 2015)
Ergot, caused by the fungal pathogen C. purpurea, has reemerged in recent years as a major problem for cereal production systems, firstly because of the problems this disease causes for F1 hybrid seed production (Mantle and Swan 1995; Miedaner et al 2010) and secondly because of new evidence that ergot alkaloids can find their way onto otherwise healthy grain (Gordon et al 2019)
Solutions to reduce ergot infection in hybrid cereal production have so far come from the deployment of pollen fertility restorer genes to maximise pollen production (Hackauf et al, 2012).Very few sources of ergot resistance per se have been identified in wheat and those that have are generally partial in effect

Summary

Introduction

Ergot, caused by the fungal pathogen Claviceps purpurea (Fr.) Tul. (Cp), is a disease of cereals and grasses that infects female flowers at anthesis (Fig. 1; Menzies and Turkington 2015). A mass of highly branched fungal hyphae, referred to as sphacelia, fills the ovule space. During this stage of infection, the fungus produces abundant asexual conidia suspended in a sugary sap that is exuded from the infected flower as honeydew (Fig. 1a). These conidia can be transported to new, uninfected flowers by rain splash and/or insects, resulting in new infections. Around 4–6 weeks after infection, an ergot sclerotium, the fungal overwintering structure (Fig. 1b), is formed in place of a seed

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