Authors: Anil Karmacharya 1, Dhondup Lhamo 2, Shaobin Zhong 3, Andrew J. Green 4, Jason D. Fiedler 5, Mingcheng Luo 1, Amanda R. Peters Haugrud 5, Elias M. Elias 4, Xiaofei Zhang 1, Yong Q. Gu 2, and Steven S. Xu 2
1. Department of Plant Sciences, University of California, Davis, CA 95616, USA
2. USDA-ARS, Crop Improvement and Genetics Research Unit, Western Regional Research Center, Albany, CA 94710, USA
3. Department of Plant Pathology, North Dakota State University, Fargo, ND 58108, USA
4. Department of Plant Sciences, North Dakota State University, Fargo, ND 58108, USA
5 USDA-ARS, Cereal Crops Research Unit, Edward T. Schafer Agriculture Research Center, Fargo, ND 58102, USA
Corresponding Author: Steven S. Xu, steven.xu@usda.gov
Presenting Author: Anil Karmacharya
Abstract
Fusarium head blight (FHB), caused by Fusarium graminearum, is currently one of the most destructive diseases affecting wheat (Triticum aestivum) and other cereal crops in North America and many regions of the world. Outbreaks of this disease can seriously impact the grain yield and end-use quality due to mycotoxin contamination. Improving FHB resistance has been a major focus in wheat genetics and breeding programs globally. However, only a few major loci have been effectively deployed, limiting progress in breeding for FHB resistance. The objectives of this study were to identify and map novel FHB resistance loci in synthetic wheat and hard red spring wheat (HRSW) germplasm using a genome-wide association study (GWAS) approach. We evaluated a panel of 274 spring wheat lines derived from backcrosses of four synthetic wheat lines from T. dicoccum (AABB) × Aegilops tauschii (DD) with eight HRSW varieties and breeding lines along with their parents for FHB response under two greenhouse seasons and four field environments over two years (2023–2024). Genotyping the population with single nucleotide polymorphism (SNP) markers generated by the 90K SNP Infinium array revealed 33,000 polymorphic markers, which were used for association mapping. A total of 16 significant marker-trait associations for FHB disease severity were identified on chromosomes 2A, 4A, 2B, 3B, 6B, 1D, 2D, and 5D, explaining 1-25% of phenotypic variation. Notably, the QTL on chromosome 4A not only has a major effect on FHB resistance but is also stable across different environments. Further validation of these QTL could facilitate successful introgression of new FHB resistance loci into breeding programs, potentially accelerating the development of FHB-resistant varieties.
ACKNOWLEDGEMENT AND DISCLAIMER
This material is based upon work supported by the U.S. Wheat & Barley Scab (USWBSI). This is a cooperative project with the U.S. Department of Agriculture and USWBSI. Any opinions, findings, conclusions, or recommendations expressed in this publication are those of the authors and do not necessarily reflect the view of the U.S. Department of Agriculture.