|WANG, Y - University Of Wisconsin|
|VANDEN LANGENBERG, K - North Carolina State University|
|WEHNER, T - North Carolina State University|
|KRAAN, P - Nunhems Seeds|
|SUELMANN, J - Nunhems Seeds|
|ZHENG, X - Magnum Seeds Inc|
|OWENS, K - Magnum Seeds Inc|
Submitted to: Plant and Animal Genome
Publication Type: Abstract Only
Publication Acceptance Date: 11/3/2015
Publication Date: 1/8/2016
Citation: Wang, Y.H., Vanden Langenberg, K., Wehner, T.C., Kraan, P., Suelmann, J., Zheng, X.Y., Owens, K., Weng, Y. 2016. QTL mapping of downy mildew resistance in PI 197088 and PI 330628 cucumbers [abstract]. Plant and Animal Genome. Paper No. P1161.
Technical Abstract: Downy mildew (DM, Pseudoperonospora cubensis) is a devastating fungal disease of cucumber worldwide. Several plant introduction lines have been identified with high resistance to the post-2004 new DM strain found in the U.S. However, the inheritance of DM resistance is still not well defined. Molecular markers that can be used for marker-assisted selection in DM resistance breeding are not widely available. Here, we report QTL mapping studies with two inbred lines PI 197088 and WI 7120 (derived from PI 330628) with high resistance against the post-2004 DM strain. Mapping populations included 154 F6 RILs from PI 197088 × Coolgreen and 243 F3 families from WI7120B × 9930. Reponses to downy mildew pathogen in artificial greenhouse or natural field inoculations of the two populations were evaluated in multiple environments over three years and four locations. Genotyping of the RIL and F3 populations was conducted with 2,086 specific-length amplified fragment (SLAF) markers and 348 SSR markers, respectively. QTL analysis identified six QTL underlying DM resistance in the RIL population contributed by PI 197088, which were located in cucumber chromosomes 1, 3, 4, and 5, respectively with 3 located in Chr5. These QTL together explained 78.4% observed phenotypic variations. With the F3 population of WI7120B × 9930, four QTL for DM resistance contributed by WI7120 were identified in chromosomes 2, 4, 5, and 6 that could explain 75.5% phenotypic variations. Based on the LOD support interval of each QTL, two QTL, one in Chr4, and the other in Chr5 seemed to be shared by PI 197088 and WI7120B although the magnitude of effects (R2) was different between the two lines at each locus.