Rebecca J. McGee, Marysia Zaleski-Cox, M. A. Jayawardana, Barry L. Tillman, Owen Wally, Laura Esquivel-Garcia, W. G. Dilantha Fernando, Harsh Raman, Harbans Bariana, Tanya Copley, Arron H. Carter, Valerio Hoyos‐Villegas
Abstract Host resistance, using qualitative genes with major effects, such as resistance ( R ) genes, is one of the most effective disease control strategies. However, because major gene‐derived resistance wanes over time, breeders must increasingly focus on quantitative trait loci and minor effect genes, which, when pyramided together, can confer stronger and longer lasting quantitative disease resistance (QDR). This review highlights the challenges of breeding for QDR in five case studies: blackleg (caused by Leptosphaeria maculans ) in canola ( Brassica napus ), white mold ( Sclerotinia sclerotiorum [ Ss ]) and common bacterial blight ( Xanthomonas citri pv . fuscans and Xanthomonas phaseoli pv. phaseoli ) in common bean ( Phaseolus vulgaris ), late leaf spot, early leaf spot, tomato spotted wilt virus, and southern stem rot in peanut ( Arachis hypogaea ), and stem, leaf, and stripe rusts ( Puccinia spp .) and powdery mildew ( Blumeria graminis ) in wheat ( Triticum aestivum ). Five emerging approaches for accelerating QDR breeding are discussed: high‐throughput phenotyping, phenomic selection, genomic selection, genome editing, and utilizing wild germplasm in pre‐breeding. Lastly, we highlight the importance for breeders of QDR to consider the phenotypic, genetic, genomic, and pathogenicity gene variation within the pathogen population, using Ss in common bean as an example. By doing so, breeders will save time and resources and develop locally adapted cultivars.