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

Abstract

Key message Four QTL for ergot resistance (causal pathogen Claviceps purpurea) have been identified in the durum wheat cultivar Greenshank. Abstract 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.

A large accessory genome and high recombination rates may influence global distribution and broad host range of the fungal plant pathogen Claviceps purpurea

“…However, the mechanisms that underlie the evolutionary success of this species is still understudied. Unlike other pathogens of cereal crops, researchers have been unsuccessful in identifying qualitative resistance genes in crop or wild grass varieties [9][10][11]. Menzies et al [9] noted the potential for a complex virulence and host susceptibility relationship of C. purpurea on durum and hexaploid wheat varieties, however, virulence was determined if sclerotia weighed > 81 mg; indicating that C. purpurea is able to initiate its biotrophic interaction but might be arrested during the final stages of sclerotia development.…”

Reprogramming of the wheat transcriptome in response to infection with Claviceps purpurea, the causal agent of ergot

“…The C. purpurea UK isolate 04–97.1 [ 79 ] were used in all inoculations. Isolate 04–97.1 was recovered from long-term glycerol stocks kept at -80 °C by inoculation onto the male sterile line two weeks prior to conidia being required.…”

Registration of durum wheat germplasm A0709‐BX05 with resistance to ergot

“…Assessments of ergot disease reaction were carried out 14 d after inoculation. Each inoculated spike was visually evaluated for honeydew resistance (honeydew production) on a scale from 1 to 4, where 1 = no honeydew, 2 = honeydew confined within glumes, 3 = honeydew exuding from the glumes in small drops, and 4 = large drops of honeydew running down the spike or dripping (Gordon et al., 2020). At maturity, plants with sclerotia protruding above the glumes of a spike were recorded.…”