A5, A7, A8, A9, D4, D5, and D11 using an F2 and a BC1S2 population derived from the cross between G. barbadense cv. Hai 7124 and G. hirsutum cv. Junmian 1 [4]. In that study, 15 resistance QTL were located on the same chromosomes using a CSIL population derived from the cross between G. barbadense cv. Hai 7124 and G. hirsutum cv. TM1, and many more resistance QTL identified were novel loci. Given that each of the CSILs used contained one and/or a few substituted segments from the donor G. hirsutum cv. TM-1, all the genetic variation between a CSIL and G. hirsutum cv. TM-1 is associated with the substituted segment(s). This circumstance minimizes
background genetic effects and allows more reliable QTL detection and PV estimation. These results showed that CSIL populations are highly effective for studying resistance http://www.selleckchem.com/products/17-AAG(Geldanamycin).html to Verticillium this website wilt. In this study, four resistance QTL were found to be located on Chr.A7, with a further three on Chr.A9. Jiang et al. [13] mapped four QTL on Chr.D7 and four on Chr.D9 for V. dahliae BP2; five QTL
on Chr.D7 and nine on Chr.D9 for V. dahliae VD8; four QTL on Chr.D7 and five on Chr.D9 for V. dahliae T9; and three QTL on Chr.D7 and seven on Chr.D7 for mixed pathogens in a F2:3 population derived from the cross between G. hirsutum cv. 60182 and G. hirsutum Thalidomide cv. Junmian 1. The QTL-mapping results revealed that QTL clusters with high additive effects were located on Chrs.A7 and A9. Bolek et al. [14] also detected three markers (CM12, STS1, and BNL3147-2) on Chr.A11 that conditioned resistance to Verticillium wilt in G. barbadense cv. Pima S-7. In the present study, one QTL for resistance to two defoliating V. dahliae isolates was found near the SSR marker BNL3147 on Chr.D11. As Chr.A11 and D11 area pair of homoeologous chromosomes, it is clear that these two homoeologous groups harbor resistance genes, and should be carefully considered in future Verticillium wilt-resistance breeding. Verticillium wilt is a destructive disease
with global consequences for cotton production. Breeding broad-spectrum cotton cultivars with resistance to this disease and others is considered to be one of the most effective means for reducing crop losses. Conventionally, breeding for disease resistance in cotton has involved selecting resistant individuals in the nursery or field from among plants suffering from serious disease. However, this approach is unsuitable for generating plants with resistance to Verticillium wilt [2]. Furthermore, no significant breakthroughs in the breeding of resistance to Verticillium wilt have been achieved for a considerable time, owing largely to a lack of germplasm known to be immune or highly resistant to this fungal pathogen.