Evaluation of Septoria Nodorum Blotch (SNB) Resistance in Glumes of Wheat (Triticum aestivum L.) and the Genetic Relationship With Foliar Disease Response.

Michael G Francki,Christopher J Mcmullan,Esther Walker,W George Morris

doi:10.3389/fgene.2021.681768

Michael G Francki, Christopher J Mcmullan + Show 2 more

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https://doi.org/10.3389/fgene.2021.681768

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Abstract

Septoria nodorum blotch (SNB) is a necrotrophic disease of wheat prominent in some parts of the world, including Western Australia (WA) causing significant losses in grain yield. The genetic mechanisms for resistance are complex involving multiple quantitative trait loci. In order to decipher comparable or independent regulation, this study identified the genetic control for glume compared to foliar resistance across four environments in WA against 37 different isolates. High proportion of the phenotypic variation across environments was contributed by genotype (84.0% for glume response and 82.7% for foliar response) with genotype-by-environment interactions accounting for a proportion of the variation for both glume and foliar response (14.7 and 16.2%, respectively). Despite high phenotypic correlation across environments, most of the eight and 14 QTL detected for glume and foliar resistance using genome wide association analysis (GWAS), respectively, were identified as environment-specific. QTL for glume and foliar resistance neither co-located nor were in LD in any particular environment indicating autonomous genetic mechanisms control SNB response in adult plants, regulated by independent biological mechanisms and influenced by significant genotype-by- environment interactions. Known Snn and Tsn loci and QTL were compared with 22 environment-specific QTL. None of the eight QTL for glume or the 14 for foliar response were co-located or in linkage disequilibrium with Snn and only one foliar QTL was in LD with Tsn loci on the physical map. Therefore, glume and foliar response to SNB in wheat is regulated by multiple environment-specific loci which function independently, with limited influence of known NE-Snn interactions for disease progression in Western Australian environments. Breeding for stable resistance would consequently rely on recurrent phenotypic selection to capture and retain favorable alleles for both glume and foliar resistance relevant to a particular environment.

Highlights

Parastagonospora nodorum (Berk.) Quaedvlieg, Verkley & Crous is the causal pathogen of Septoria nodorum blotch (SNB) of wheat that infects the lower leaves of the canopy and is identified by dark brown round or lens shaped spots that coalesce and develop black pycnidia as lesions mature (Eyal et al, 1987)
The trial at South Perth in 2020, provided an opportunity to compare the response of 232 wheat lines to glume and foliar SNB infection under different climatic environments
The outcome of this study confirms an independent genetic relationship between glume and foliar response when wheat lines were evaluated at any particular location, evident by the lack of single nucleotide polymorphic (SNP) markers associated with QTL that were neither co-located nor in LD

Summary

Introduction

Parastagonospora (syn. ana, Stagonospora; teleo, Phaeosphaeria) nodorum (Berk.) Quaedvlieg, Verkley & Crous is the causal pathogen of Septoria nodorum blotch (SNB) of wheat that infects the lower leaves of the canopy and is identified by dark brown round or lens shaped spots that coalesce and develop black pycnidia as lesions mature (Eyal et al, 1987). Ana, Stagonospora; teleo, Phaeosphaeria) nodorum (Berk.) Quaedvlieg, Verkley & Crous is the causal pathogen of Septoria nodorum blotch (SNB) of wheat that infects the lower leaves of the canopy and is identified by dark brown round or lens shaped spots that coalesce and develop black pycnidia as lesions mature (Eyal et al, 1987). Foliar symptoms in Western Australia (WA) are seen at tillering (Feekes 5) and is a precursor to glume infection. Infected heads will turn dark brown often with a purple tint and black pycnidia evident as typical glume blotch symptoms (Eyal et al, 1987). Breeding for leaf and glume blotch resistance is challenging due to the inherent genetic complexity controlling SNB response when the disease is most damaging (reviewed in Francki, 2013)

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