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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 #322773

Research Project: Genetic Improvement of Durum and Spring Wheat for Quality and Resistance to Diseases and Pests

Location: Cereal Crops Research

Title: Genetic relationships between race-nonspecific and race-specific interactions in the wheat-Pyrenophora tritici-repentis pathosystem

Author
item Kariyawasam, Gayan - North Dakota State University
item Carter, Arron - Washington State University
item Rasmussen, Jack - North Dakota State University
item Faris, Justin
item Xu, Steven
item Mergoum, Mohamed - North Dakota State University
item Liu, Zhaohui - North Dakota State University

Submitted to: Theoretical and Applied Genetics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/9/2016
Publication Date: 1/21/2016
Publication URL: http://handle.nal.usda.gov/10113/62923
Citation: Kariyawasam, G.K., Carter, A.H., Rasmussen, J.B., Faris, J., Xu, S.S., Mergoum, M., Liu, Z. 2016. Genetic relationships between race-nonspecific and race-specific interactions in the wheat-Pyrenophora tritici-repentis pathosystem. Theoretical and Applied Genetics. 129:897-908. doi: 10.1007/s00122-016-2670-x.

Interpretive Summary: Tan spot is an important fungal disease of wheat worldwide, and it has the ability to cause significant yield losses in susceptible varieties when inoculum levels are high. Genetic resistance is the most feasible means of reducing losses due to tan spot. Previous genetic research has shown that the tan spot produces proteins known as necrotrophic effectors (e.g. Ptr ToxA and Ptr ToxC) that cause disease on wheat plants that contain specific genes (e.g. Tsn1 and Tsc1) that recognize the proteins, and thus elimination of these genes from wheat can lead to enhanced levels of resistance. However, few active genes that condition high levels of broad spectrum resistance to tan spot have been identified. In this research, wheat lines were evaluated for reaction to various strains of the tan spot pathogen to identify genes that may confer high levels of broad spectrum resistance. Using DNA markers and genetic mapping, a gene with major effects for tan spot resistance to all strains was identified on chromosome 3B in the wheat variety Penawawa. Genetic analysis indicated that this gene precluded susceptibility caused when Ptr ToxA was recognized by Tsn1, but not susceptibility caused when Ptr ToxC was recognized by the wheat gene Tsc1. Two other genes with relatively subtle effects on tan spot resistance were also identified in Penawawa, but on different chromosomes. The tan spot resistance gene identified on chromosome 3B and the DNA markers associated with it will be very useful for wheat breeders to develop tan spot resistant varieties efficiently.

Technical Abstract: Tan spot, caused by the fungus Pyrenophora tritici-repentis, is a destructive disease of wheat worldwide. The disease system is known to include inverse gene-for-gene, race specific interactions involving the recognition of fungal-produced necrotrophic effectors (NEs) by corresponding host sensitivity genes. However, quantitative trait loci (QTLs) conferring race-nonspecific resistance have also been identified. In this work, we identified a major race-nonspecific resistance QTL and characterized its genetic relationships with the NE-host gene interactions Ptr ToxA-Tsn1 and Ptr ToxC-Tsc1 in a recombinant inbred wheat population derived from the cross between ‘Louise’ and ‘Penawawa.’ Both parental lines were sensitive to Ptr ToxA, but Penawawa and Louise were highly resistant and susceptible, respectively, to conidial inoculations of all races. Resistance was predominantly governed by a major race-nonspecific QTL on chromosome arm 3BL for resistance to all races and a QTL at the distal end of chromosome arm 1AS for resistance to the Ptr ToxC-producing isolates, which corresponded to the known location of the Tsc1 locus. The effects of the 3B and 1A QTLs were largely additive, and the 3B resistance QTL was epistatic to the Ptr ToxA-Tsn1 interaction. Resistance to race 2 in F1 plants was completely dominant, however race 3-inoculated F1 plants were only moderately resistant because they developed chlorosis presumably due to the Ptr ToxC-Tsc1 interaction. This work provides further understanding of genetic resistance in the wheat-tan spot system as well as important guidance for tan spot resistance breeding.