Genetics, Breeding, and Marker‐Assisted Selection for Verticillium Wilt Resistance in Cotton

Abstract

Verticillium wilt (VW), caused by the soil‐borne fungus Verticillium dahliae Kleb., is one of the most destructive diseases in Upland cotton (Gossypium hirsutum L.) production in the U.S. and worldwide. Development of VW‐resistant cultivars remains the only economic option for controlling the disease. The objective of this review was to summarize the progress in screening methods, resistance sources, and genetics, quantitative trait locus (QTL) mapping, marker‐assisted selection (MAS) and breeding for VW resistance in cotton. Even though Gossypium barbadense L. carries high levels of resistance, its resistance has not been transferred into commercial Upland cultivars. Many Acala cotton cultivars developed in New Mexico and California between the 1940s and the 1990s, and some commercial transgenic cultivars are tolerant or moderately resistant to VW. However, due to difficulties in achieving consistent and uniform inoculation and infection with V. dahliae, both qualitative and quantitative inheritance of VW resistance have been reported in numerous studies for resistant G. barbadense and Upland genotypes. Several QTL analyses have shown the existence of VW resistance QTLs on almost all the tetraploid cotton chromosomes; however, QTLs have most frequently been detected on c5, c7, c8, c11, c16, c17, c19, c21, c23, c24, and c26. This has led to MAS for progeny with favorable QTL alleles for VW resistance in several experiments. Phenotypic selection for VW resistance has been inefficient, while the effectiveness and efficiency of MAS remain to be validated. There is an urgent need for the development of better plant inoculation and screening methods, and for more molecular mapping studies to discern the genetic basis of VW resistance in cotton.

Quantitative Trait Locus Mapping for Verticillium wilt Resistance in an Upland Cotton Recombinant Inbred Line Using SNP-Based High Density Genetic Map

“…More than 100 QTLs related to VW have been detected on most of the 26 tetraploid cotton chromosomes except on chromosomes c6, c10, c12, and c18 (Zhang et al, 2014a,b, 2015). In this study, VW QTLs with minor contributions to the observed PV were detected on these four chromosomes.…”

“…For the strain V991, 3 VW QTLs have been previously mapped on c9, c17, and c23 using a RIL population from Prema × 86-1 (Ning et al, 2013) and 2 QTLs on c6 and c21 using a F2:3 population (Zhang et al, 2014a). In this study, VW strain V991 resistance QTLs were identified on c1, c5, c10, c14, c15, c17, c20, c22, c25 for DI and on c2-c4, c7, c10, c11, c14, c15, c17, c21, and c22 for DInc.…”

“…Most of the studies have reported the difficulty to reliably identify VW QTLs because of the likely relatively low contribution of each QTL to the phenotype and the low genome coverage (Zhang et al, 2014a). In this study, the high-density SNP markers used provided us a higher genome coverage allowing higher resolution in the VW QTLs mapping.…”

“…In the intraspecific crosses of upland cotton, different inheritance patterns have been reported (Barrow, 1970; Mert et al, 2005; Cai et al, 2009; Zhang et al, 2014a). This controversies may be incurred by the different resistance sources and homozygosity of resistance genes, virulence and inoculum levels of the pathogen, evaluation methods, environmental factors (especially soil temperature and moisture), and plant maturity (Zhang et al, 2014a). Moreover, VW resistance has been reported to be under the control of recessive genes (Roberts and Staten, 1972; Devey and Roose, 1987).…”

“…VW resistant QTLs have been identified on almost all the cotton chromosomes except on c10 and c18 using mainly interspecific and very few intraspecific of upland cotton populations (Jian et al, 2003; Mert et al, 2005; Fang et al, 2013b; Wang et al, 2014; Zhang et al, 2014a, 2015). A major QTL conferring resistance and explaining 23.1–27.1% of the observed phenotypic variations (PVs) to the VW defoliating strain V991 was identified on c6 in LHB22 × Jimian11 F 2:3 population and was confirmed in LHB22 × NNG F 2:3 population.…”