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ARS Home » Pacific West Area » Pullman, Washington » Wheat Genetics, Quality Physiology and Disease Research » Research » Publications at this Location » Publication #199369


item Santra, D
item Santra, M
item Uauy, C
item Garland-campbell, Kimberly
item Chen, Xianming
item Dubcovsky, J
item Kidwell, K

Submitted to: Plant and Animal Genome VX Conference Abstracts
Publication Type: Abstract Only
Publication Acceptance Date: 9/1/2005
Publication Date: 1/1/2006
Citation: Santra, D.K., Santra, M., Uauy, C., Garland Campbell, K.A., Chen, X., Dubcovsky, J., Kidwell, K.K. 2006. Identifying qtl for high-temperature adult-plant resistance to stripe rust in wheat (triticum aestivum l.). Plant and Animal Genome Abstracts. Page 179. Jan 14-18, 2006, San Diego, CA.

Interpretive Summary:

Technical Abstract: High-temperature, adult-plant (HTAP) resistance to stripe rust in wheat is governed by multiple genes, which are race non-specific and durable. The winter wheat cultivar ‘Stephens’ has served as the primary source of HTAP resistance in the Pacific Northwest region of the U.S. for the last 28 years. The objectives of this study were to: (1) identify and map QTL for HTAP resistance to stripe rust in Stephens through genetic linkage analysis; and (2) develop DNA markers for use in marker-assisted breeding. Three hundred recombinant inbred lines (RILs) were developed from reciprocal crosses between Stephens (resistant) and Michigan Amber (susceptible). F5, F6, and F7 RIL derivatives were evaluated for three years at one location, whereas F8 derivatives were evaluated at four locations in one year. Area under disease progression curve (AUDPC) values were calculated for each RIL using disease infection type and percentage of infected leaf area recorded on three different dates for each site year. AUDPC data from a subset of 114 RILs that were evaluated with 375 polymorphic DNA (250 RGA, 124 SSR and 1 STS) markers were used for genetic linkage map construction and QTL mapping. Three major QTL associated with HTAP resistance were identified; however, variation in the level of significance of associations was detected among locations and across years. Q.htap-1 (LOD=6.45-14.58, R2=0.23-0.44, P<0.0001) and Q.htap-2 (LOD=5.54-7.74, R2=0.20-0.26, P<0.0001) were detected on chromosome 6BS within a 23.1 cM region flanked by Xgwm88.2 and Xucw71 and a 14.9 cM region flanked by Xgwm508.2 and Xgwm13, respectively, whereas, Q.htap-3 (LOD 2.4-5.4, R2=0.09-0.20, P<0.0001) mapped within a 45.2cM region flanked by XwlSAS5 and Xbarc243 on 5B. Our ability to detect QTL associated with HTAP resistance was greatly influenced by changes in pathogen race structure over time.