Novel sources of resistance to Septoria nodorum blotch in the Vavilov wheat collection identified by genome-wide association studies

Huyen T T Phan,Lee T Hickey,Eiko Furuki,Kar-Chun Tan,Kasia Rybak,Richard P Oliver,Eric Dinglasan,Stefania Bertazzoni

doi:10.1007/s00122-018-3073-y

Huyen T T Phan, Lee T Hickey + Show 6 more

Open Access

https://doi.org/10.1007/s00122-018-3073-y

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Abstract

Key messageThe fungus Parastagonospora nodorum causes Septoria nodorum blotch (SNB) of wheat. A genetically diverse wheat panel was used to dissect the complexity of SNB and identify novel sources of resistance.The fungus Parastagonospora nodorum is the causal agent of Septoria nodorum blotch (SNB) of wheat. The pathosystem is mediated by multiple fungal necrotrophic effector–host sensitivity gene interactions that include SnToxA–Tsn1, SnTox1–Snn1, and SnTox3–Snn3. A P. nodorum strain lacking SnToxA, SnTox1, and SnTox3 (toxa13) retained wild-type-like ability to infect some modern wheat cultivars, suggesting evidence of other effector-mediated susceptibility gene interactions or the lack of host resistance genes. To identify genomic regions harbouring such loci, we examined a panel of 295 historic wheat accessions from the N. I. Vavilov Institute of Plant Genetic Resources in Russia, which is comprised of genetically diverse landraces and breeding lines registered from 1920 to 1990. The wheat panel was subjected to effector bioassays, infection with P. nodorum wild type (SN15) and toxa13. In general, SN15 was more virulent than toxa13. Insensitivity to all three effectors contributed significantly to resistance against SN15, but not toxa13. Genome-wide association studies using phenotypes from SN15 infection detected quantitative trait loci (QTL) on chromosomes 1BS (Snn1), 2DS, 5AS, 5BS (Snn3), 3AL, 4AL, 4BS, and 7AS. For toxa13 infection, a QTL was detected on 5AS (similar to SN15), plus two additional QTL on 2DL and 7DL. Analysis of resistance phenotypes indicated that plant breeders may have inadvertently selected for effector insensitivity from 1940 onwards. We identify accessions that can be used to develop bi-parental mapping populations to characterise resistance-associated alleles for subsequent introgression into modern bread wheat to minimise the impact of SNB.

Highlights

The aim of this study is to use a combination of wheat diversity, P. nodorum strains differing in effector gene profile and Genome-wide association studies (GWAS) to further dissect the complexity of Septoria nodorum blotch (SNB) in the presence and absence of SnToxA–Tsn1, SnTox1–Snn1, and SnTox3–Snn3 interactions
It was previously demonstrated that P. nodorum toxa13 remained fully pathogenic on three major Australian wheat cultivars (Tan et al 2015)
SNB is a recalcitrant disease in many parts of the world

Summary

Introduction

The pathogen causes foliar and glume damage that results in significant yield losses in many wheat growing areas around the world (Eyal et al 1987; Oliver et al 2009). SNB is largely governed by a series of proteinaceous fungal necrotrophic effectors (NEs) that cause necrosis and/or chlorosis on wheat lines possessing matching dominant susceptibility genes through effector-triggered susceptibility (Tan et al 2010). Three single copy genes that encode NEs have been identified in P. nodorum. SnToxA encodes a 13.2 kDa mature protein. Tsn encodes a nucleotide binding site leucine-rich repeat protein with a protein kinase domain (Faris et al 2010). SnTox encodes a 10.3 kDa small cysteine-rich protein with a putative chitin-binding domain.

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