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Title:   Author  item
                                            Ulloa, Mauricioitem
                                            WANG, C. - University Of Californiaitem
                                            ROBERTS, P. - University Of California
  Submitted to: Plant Breeding
                                    Publication Type: Peer Reviewed Journal
                                    Publication Acceptance Date: 8/21/2009
                                    Publication  Date: 10/30/2010
                                    Citation: Ulloa, M., Wang, C., Roberts, P.A. 2010. Gene action analysis by inheritance and QTL mapping of resistance to root-knot nematodes in cotton. Plant Breeding. 129(5):541-550.Interpretive Summary: The southern root-knot nematode (RKN) is a soil inhabiting worm that damages cotton directly and forms a disease complex with the fungus causing Fusarium wilt. This complex results in severe yield loss in some growing regions in the U.S. Host-plant resistance is highly effective in preventing crop loss from the nematode-fusarium complex. In addition, molecular markers can be powerful tools for identifying RKN resistant cottons, reducing dependence on laborious field and greenhouse evaluations. A molecular marker is a small piece of DNA that can be detected chemically. To better understand host-plant mechanisms of defense, we investigated the RKN resistance gene interactions, and how these genes are transmitted to progeny in several cotton types with different RKN resistance backgrounds. Differences between the studied cottons indicated that gene interactions influenced their responses to nematode injury. We concluded that breeding for optimal resistance must be based on selection of progenies with combinations of genes for resistance. Selection success rate using molecular markers was more than 85 percent for identifying resistant cottons. The findings from this research confirmed the importance of a major DNA region on chromosome 11 harboring RKN resistance genes. In addition, the studied markers can be used to identify cottons with RKN resistant genes, thereby speeding development and release of resistant varieties for USA cotton growers.
                                Technical Abstract: Host-plant resistance is highly effective in controlling crop loss from nematode infection. In addition, molecular markers can be powerful tools for marker-assisted selection (MAS), where they reduce laborious greenhouse phenotype evaluation to identify root-knot nematode (RKN) Meloidogyne incognita Kofoid and White (Chitwood) resistant genotypes. To better understand host-plant interactions, we investigated gene action and genomic locations of RKN resistance genes in cotton (Gossypium hirsutum L). Twelve parents, 17 intraspecific (G. hirsutum x G. hirsutum) and four interspecific (G. hirsutum x G. barbadense L.) F1, and 11 F2 populations were investigated by examining different RKN resistance backgrounds. The F1 and F2 generation means and distributions, and differences between F1 and mid-parent values indicated that allelic interaction, epistasis, and heterosis operated in these crosses for galling index (GI). Genetic and QTL analyses in crosses NemX x SJ-2 and SJ-2 x Clevewilt revealed resistance due to at least one major recessive QTL with strong additive effect, while in NemX x PS 7 resistance was due to at least one major QTL with strong dominant effect. SSR markers CIR316 and MUCS088 on chromosomes 11 and 21 showed the association of two different chromosomes with the RKN resistance, supporting the gene interactions observed by the significant differences between generation means. This also supports the two gene model of observed resistant:susceptible ratios in F2 and F3 (PS 7 x NemX) populations. Selection success rate for MAS was > 85% for identifying resistant genotypes with GI < 3 from these crosses with SSR CIR316, BNL1231 and MUCS088, and CAPS (GHACC1). QTL analyses validated the importance of a major genome-telomeric region on chromosome 11, harboring RKN genes, rkn1 and RKN2 based on different RKN resistance backgrounds. We conclude that breeding for optimal resistance must be based on selection of progenies with combinations of determinant genes homozygous for resistance.


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