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ARS Home » Plains Area » Fargo, North Dakota » Edward T. Schafer Agricultural Research Center » Cereal Crops Research » Research » Publications at this Location » Publication #347510

Title: A major tan spot race-nonspecific resistance gene in tetraploid and hexaploid wheat

item Faris, Justin
item Overlander-Chen, Megan
item KARIYAWASAM, GAYAN - North Dakota State University
item CARTER, ARRON - Washington State University
item LIU, ZHAOHUI - North Dakota State University

Submitted to: Plant and Animal Genome Conference
Publication Type: Abstract Only
Publication Acceptance Date: 11/2/2017
Publication Date: 1/13/2018
Citation: Faris, J.D., Overlander, M., Kariyawasam, G.K., Carter, A.H., Liu, Z. 2018. A major tan spot race-nonspecific resistance gene in tetraploid and hexaploid wheat [abstract]. Plant and Animal Genome Conference XXVI. January 13-17, 2018, San Diego, CA. P1080.

Interpretive Summary:

Technical Abstract: Tan spot, caused by the necrotrophic fungus Pyrenophora tritici-repentis (Ptr), is a major foliar disease of both common and durum wheat. Over the past few decades, research has revealed that wheat-Ptr interactions are based on an inverse gene-for-gene system, where pathogen-secreted necrotrophic effectors (also known as host-selective toxins) induce susceptibility when recognized by dominant sensitivity genes in the host. However, a few race-nonspecific resistance QTLs have also been reported. In 2005, Faris and Friesen reported a race-nonspecific QTL with major effects on chromosome 3B in the Brazilian hard red spring wheat line BR34, and Kariyawasam et al. (2016) reported a QTL in the same region in the soft white spring wheat cultivar ‘Penawawa’. Here, we evaluated the Langdon durum–Triticum dicoccoides accession Israel-A chromosome substitution lines (LDN-DIC) for reaction to all races. With the exception of LDN-DIC 3B being highly resistant, LDN and all the LDN-DIC lines were moderately to highly susceptible. A recombinant inbred chromosome line population derived from LDN x LDN-DIC 3B was used to map the location of a single dominant resistance gene using SSR markers. In addition, chromosome 3B linkage maps in the BR34- and Penawawa-derived mapping populations were reconstructed using the Illumina 90K SNP array and SSRs, and the disease data was reanalyzed. Detailed analysis indicated that BR34, Penawawa, and T. dicoccoides accession Israel-A all possess the same chromosome 3B tan spot resistance gene. Current progress on marker development and deployment of the gene will be presented.