|WANG, CONGLI - University Of California|
|HUTMACHER, ROBERT - University Of California|
|WRIGHT, STEVEN - University Of California|
|DAVIS, R. MICHAEL - University Of California|
|SASKI, CHRISTOPHER - Clemson University|
|ROBERTS, PHILIP - University Of California|
Submitted to: Molecular Genetics and Genomics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/28/2011
Publication Date: 6/27/2011
Citation: Ulloa, M., Wang, C., Hutmacher, R.B., Wright, S.D., Davis, R.M., Saski, C.A., Roberts, P.A. 2011. Mapping Fusarium wilt race 1 resistance genes in cotton by inheritance, QTL and sequencing composition. Molecular Genetics and Genomics. 286:21-36.
Interpretive Summary: Fusarium wilt is an important disease that reduces yield in cotton. This disease is caused by a fungus that can survive for long periods in the soil, making it impossible to eliminate. Studies of Upland and Pima cottons identified a major resistance gene for race 1 of the Fusarium wilt fungus. This major resistance gene was found to play a significant role in conferring resistance in different cotton genetic backgrounds. We suggest that this gene should be a primary target for breeding Fusarium-resistant cotton. Analyses also indicated the involvement in Fusarium resistance of additional genes on five cotton chromosomes. Finally, we identified molecular markers (small pieces of DNA that can be detected chemically) associated with Fusarium wilt race 1 resistance. These molecular markers should be useful for breeding Fusarium wilt resistance into elite cotton cultivars by marker-assisted selection. In addition to their importance to Fusarium wilt resistance, the genes and molecular markers we identified may be useful in identifying resistance to other cotton diseases.
Technical Abstract: Host-plant resistance is highly effective in limiting yield loss in cotton (Gossypium spp.) from Fusarium wilt [Fusarium oxysporum f.sp. vasinfectum (FOV) Atk. Sny & Hans]. In this study, we conducted a comprehensive analysis of gene action in cotton governing FOV race 1 resistance by applying molecular markers to F2 and recombinant inbred line (RIL) interspecific mapping populations generated from the crosses Pima-S7 (G. barbadense L.) x ‘Acala NemX’ (G. hirsutum L.) and Upland TM-1 (G. hirsutum) x Pima 3-79 (G. barbadense), respectively. Parents and populations were evaluated for disease severity index (DSI) of leaves, and vascular stem and root staining (VRS) in three greenhouse tests and one field test. Sequential evaluations of DSI and VRS after inoculation were used to measure disease progress. A single resistance gene model was observed for the F2 population based on inheritance of phenotypes, but additional inheritance analyses and QTL mapping indicated the involvement of multiple genes. A set of 24 SSR markers indicated gene interactions and inheritance from nine cotton chromosomes, with major QTLs detected on five chromosomes (C06, C08, C011, C016, and C019) based on DSI or VRS. The Fov1-C06 locus explained up to 22.3% of DSI variation; the Fov1-C081 locus 10.6%; the Fov1-C0111 locus 12.3% and Fov1-C0112 locus 14.2%; in VRS the Fov1-C016 locus explained 31% of the variation; and in DSI the Fov1-C019 locus explained 13%. The FOV1 locus previously identified in Pima-S7 using AFLP markers, was mapped to chromosome 16 and co-located with the Fov1-C016 QTL in the TM-1 x Pima 3-79 RIL. We conclude that this QTL has a significant role in conferring FOV race 1 resistance in different cotton backgrounds and should be a primary target for breeding with marker assisted selection. Reported gene sequences may be involved in resistance to FOV infection and possibly other common soil pathogens. In addition, reconciliation between genetic and physical mapping of gene annotations from new DNA sequences of BAC clones tagged with the resistance-associated QTL markers revealed gene regions rich in disease-response elements.