Breeding, Genetics, and Quantitative Trait Locus Mapping for Fusarium Wilt Resistance in Cotton

Abstract

ABSTRACT Fusarium wilt (FW), caused by the soilborne fungus Fusarium oxysporum f. sp. vasinfectum (FOV), with eight races recognized, is one of the most destructive diseases in cotton ( Gossypium spp.). Employment of FW‐resistant cultivars has proven to be the most cost‐effective method to control the disease. This review provides a comprehensive synthesis of research progress in breeding, genetics, and molecular mapping of FW resistance. A focused pedigree analysis in Upland cotton ( G. hirsutum L.) has identified five major FW‐resistant sources (‘Dillon’, ‘Dixie Triumph’, ‘Cook 307‐6’, ‘Coker Clevewilt’, and ‘Wild’) in the United States and three (‘Chuan 52‐128’, ‘Chuan 57‐681’, and ‘CRI 12’) in China. The use of numerous early segregating populations has consistently confirmed the predominant presence of additive gene effects on FW resistance; however, heritability is usually low because of high experimental error. Several mapping studies have detected approximately 40 quantitative trait loci (QTL) on 19 chromosomes. A number of qualitative genetic studies have identified five major resistance genes in Upland and Pima ( G. barbadense L.) cotton including Fw1 , Fw2 , Fw R (chromosome 17), FOV1 (chromosome 16), and FOV4 (chromosome 14). There are other major resistance genes identified through marker or segregating analysis, but methods with high and uniform infection by FOV are required to confirm the results. More differential hosts should be developed to differentiate new races, and more resistance genes from new sources should be identified for their strategic deployment in preventing a possible risk of disease epidemic.