Poster # 312

Lanfei Zhao ^1,2, Amy Bernardo ³, Fanmei Kong ^1,2, Wei Zhao ^1,2, Yanhong Dong ⁴, Harold N. Trick ⁵, Hyeonju Lee ⁵, Jessica Rupp ⁵, Guihua Bai ^1,3
1. Department of Agronomy, Kansas State University, 2004 Throckmorton Hall, Manhattan, KS 66506, USA
2. National Key Laboratory of Wheat Improvement, Shandong Key Laboratory of Wheat Improvement, College of Agronomy, Shandong Agriculture University, Taian, Shandong, China 271018
3. USDA, Hard Winter Wheat Genetics Research Unit, 4008 Throckmorton Hall, Manhattan, KS 66506, USA
4. Department of Plant Pathology, University of Minnesota, St. Paul, MN 55108, USA
5. Department of Plant Pathology, Kansas State University, 4024 Throckmorton Hall, Manhattan, KS 66506, USA.
Corresponding Author: Guihua Bai, guihua.bai@usda.gov

Lanfei Zhao

Fusarium head blight (FHB), mainly incited by Fusarium graminearum Schwabe, has caused great losses in grain yield and quality of wheat and barley globally. Fhb7, a major gene for FHB resistance, has been cloned and found to encode a glutathione S-transferase (GST). Fhb7 originated from 7E chromosome of Thinopyrum ponticum and confers broad resistance to Fusarium species. However, some recent reports raised doubt about whether GST is the causal gene of Fhb7. To validate the gene function of GST in wheat, we phenotyped Fhb7 near-isogenic lines (Jimai22-Fhb7 vs Jimai22) and GST over-expression lines for FHB resistance. The Fhb7 NILs were planted in the Kansas State University FHB nursery in 2018 and 2020. Jimai22-Fhb7 showed significantly higher FHB resistance with a lower PSS, FDK and DON concentration than susceptible Jimai22. In the GST transgenic lines, GST was highly overexpressed in almost all the positive transgenic lines driven by either the maize ubiquitin promoter (MubiP) or its native promoter (NP) in the wheat cultivar ‘Fielder’ and those transgenic T₂ plants showed high FHB resistance. Only one MubiP-driven transgenic line showed low GST expression and similar susceptibility as Fielder, suggesting high GST expression confers Fhb7 FHB resistance. We also knocked out GST in Jimai22-Fhb7 line using the CRISPR-Cas9-mediated gene-editing. The GST-knockout lines showed significantly higher FHB susceptibility compared with the non-edited control plants. Therefore, GST is the causal gene of Fhb7 FHB resistance and its gene expression level significantly infects the gene function in FHB resistance.