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TECHNICAL SESSION: Mycology

Identification of septoria nodorum blotch sensitivity genes in hard winter wheat

Monday, August 4, 2025
12:45 PM - 1:00 PM HST
Location: Room 311

    Presenting Author(s)

  • AA

    Anju Maan Ara

    Graduate Research Assistant
    Oklahoma State University
    Stillwater, Oklahoma, United States

    • Author(s)

  • BC

    Brett F. Carver

    Rgts Prof/Enwd Ch
    Oklahoma State University
    Stillwater, Oklahoma, United States

  • TF

    Timothy L. Friesen

    USDA-ARS
    Fargo, North Dakota, United States

  • DH

    Danielle Holmes

    USDA-ARS
    Fargo, North Dakota, United States

  • GB

    Guihua Bai

    USDA-ARS Hard Winter Wheat Genetics Research Unit
    Manhattan, Kansas, United States

  • PS

    Paul St. Amand

    USDA-ARS Hard Winter Wheat Genetics Research Unit
    Manhattan, Kansas, United States

  • AB

    Amy Bernardo

    Kansas State University
    Manhattan, Kansas, United States

  • MA

    Meriem Aoun

    Oklahoma State University
    Stillwater, Oklahoma, United States

Abstract Text:

The necrotrophic fungus Parastagonospora nodorum is the causal agent of septoria nodorum blotch (SNB) of wheat.  The P. nodorum effectors recognition by wheat sensitivity genes leads to susceptibility. Limited information exists on SNB sensitivity genes in contemporary U.S. hard winter wheat (HWW). The objective of this study was to determine the prevalence of SNB sensitivity genes in 619 HWW breeding lines and cultivars from the Oklahoma State University wheat breeding program. This HWW panel was evaluated against five P. nodorum isolates and five effectors ToxA, Tox1, Tox3, Tox5, and Tox267. The panel was genotyped using genotyping-by-sequencing (GBS) and diagnostic markers for the sensitivity genes Tsn1 and Snn1. Genome wide association studies (GWAS) were conducted using phenotypic data, 34357 single nucleotide polymorphism (SNP) markers generated from GBS, and markers linked to Tsn1 and Snn1. Evaluations against P. nodorum isolates showed that 28-77% of the genotypes were resistant, depending on the isolates. Toxin infiltration assays showed that 55%, 6%, and 44% of the genotypes were sensitive to ToxA, Tox1, and Tox3, respectively. Tox5 and Tox 267 infiltration assays are ongoing. Diagnostic markers showed that 45% and 73% of the genotypes lacked Tsn1 and Snn1, respectively. GWAS identified SNPs linked to Tsn1, Snn1, and Snn3-B1 associated with ToxA, Tox1, and Tox3 responses, respectively. Tsn1 had the largest effect in explaining sensitivity to P. nodorum isolates. Eliminating SNB sensitivity genes, especially Tsn1 will enhance SNB resistance in HWW.