|Bolek, Yuksel - KAHRAMANMARAS SUTCU IMAM|
|El-Zik, Kamal - TEXAS A&M UNIVERSITY|
|Pepper, Alan - TEXAS A&M UNIVERSITY|
|Magill, Clint - TEXAS A&M UNIVERSITY|
|Thaxton, Peggy - TEXAS A&M UNIVERSITY|
|Reddy, O. Umesh - WEST VIRGINIA STATE UNIV|
Submitted to: Plant Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: February 18, 2005
Publication Date: April 4, 2005
Citation: Bolek, Y., El-Zik, K.M., Pepper, A.E., Bell, A.A., Magill, C.W., Thaxton, P.M., Reddy, O.K. 2005. Mapping of Verticillium wilt resistance genes in cotton. Plant Science. 168:1581-1590. Interpretive Summary: Breeding for resistance to Verticillium wilt in cotton germplasm is complicated by the incomplete expression of resistance and its extreme sensitivity to temperature. Unusually warm or cold weather late in the growing season may largely mask the differential expression of resistance in siblings causing valuable resistance to be lost. If molecular markers were available to locate resistance genes, breeding for resistance to wilt could be facilitated and specific resistance genes could be tracked. In this study, genes responsible for resistance in the cultivar Pima S-7 were shown to reside on chromosome 11 and were located in two linkage groups, LG-1 and LG-2. These studies provide bases for development of highly specific markers that can be used in a breeding program.
Technical Abstract: Cotton quality and yield are affected by several factors during the growing season. A soil inhabiting fungus, Verticillium dahliae Kleb., can cause substantial yield loss in cotton. A molecular mapping F2 population derived from the interspecific cross of the highly tolerant Gossypium barbadense cv. Pima S-7 and the susceptible G. hirsutum cv. Acala 44 was phenotyped for disease incidence and severity. Phenotyping of individual plant reactions to the disease was quantified using a set of growth parameters measured 3 weeks after inoculation. The F2 phenotypic distribution of these parameters (number of healthy leaves, node number, leaf weight, stem weight, and total shoot weight) suggested that resistance is polygenic inherited. Microsatellites were used to reveal polymorphism between resistant and susceptible parents. A total of 255 simple sequence repeat (SSR) primer pairs were screened over bulks constituted by 10 resistant and 10 susceptible progeny. Sixy markers were used to analyze quantitative trait loci (QTLs). Eleven linkage groups were constructed consisting of 35 markers and spanning 531 cM with an average distance of 15.17 cM. QTL analysis was performed with MapQTL and QTL Cartographer. MapQTL indicated that 15 markers have significant linkage associations and 9 were distributed to chromosomes 10, 11, 12, and 25. Interval mapping also indicated the most likely position of markers that are significant and located on linkage groups. Three loci (CM12, STS1, 3147-2) had large effect on resistance to Verticillium wilt. Two loci were located on LG-1 and one on LG-2 and both linkage groups are located on chromosome 11.