Open AccessGenome‐wide Association Mapping and Prediction of Adult Stage Septoria tritici Blotch Infection in European Winter Wheat via High‐Density Marker Arrays
Author(s) -
Muqaddasi Quddoos H.,
Zhao Yusheng,
Rodemann Bernd,
Plieske Jörg,
Ganal Martin W.,
Röder Marion S.
Publication year - 2019
Publication title -
the plant genome
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 41
ISSN - 1940-3372
DOI - 10.3835/plantgenome2018.05.0029
Subject(s) - septoria , biology , winter wheat , mycosphaerella graminicola , stage (stratigraphy) , genome wide association study , agronomy , genetics , gene , single nucleotide polymorphism , genotype , paleontology
Septoria tritici blotch (STB) caused by the fungus Zymoseptoria tritici is a devastating foliar disease of wheat ( Triticum aestivum L.) that can lead to substantial yield losses. Quantitative genetic resistance has been proposed as a durable strategy for STB control. In this study, we dissected the genetic basis of STB infection in 371 European wheat varieties based on 35k and 90k single nucleotide polymorphism marker arrays. The phenotypic data analyses suggested that large genetic variance exists for STB infection with a broad‐sense heritability of 0.78. Genome‐wide association studies (GWAS) propose the highly quantitative nature of STB infection with potential associations on chromosomes 1A, 1B, 2D, 4A, 5A, 6A, 6D, 7A, and 7B. Increased marker density in GWAS by combining markers from both arrays helped to detect additional markers explaining increased genotypic variance. Linkage disequilibrium analyses revealed genes with a possible role in disease resistance. The potential of genomic prediction (GP) assessed via two models accounting for additive effects and additive plus epistatic interactions among the loci suggested the possibility of genomic selection for improved STB resistance. Genomic prediction results also indicated that the higher‐order epistatic interactions are not abundant and that both marker platforms are equally suitable for GP of STB infection. Our results provide further understanding of the quantitative genetic nature of STB infection, serve as a resource for marker‐assisted breeding, and highlight the potential of genomic selection for improved STB resistance.