|LIU, ZHAOLIU - North Dakota State University|
|ZURN, JASON - North Dakota State University|
|KARIYAWASAM, GAYAN - North Dakota State University|
|SHI, GONGJUN - North Dakota State University|
|HANSEN, JANA - North Dakota State University|
|RASMUSSEN, JACK - North Dakota State University|
|ACEVEDO, MARICELIS - North Dakota State University|
Submitted to: Theoretical and Applied Genetics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/21/2017
Publication Date: 3/14/2017
Publication URL: http://handle.nal.usda.gov/10113/5700705
Citation: Liu, Z., Zurn, J.D., Kariyawasam, G., Faris, J.D., Shi, G., Hansen, J., Rasmussen, J.B., Acevedo, M. 2017. Inverse gene-for-gene interactions contribute additively to tan spot susceptibility in wheat. Theoretical and Applied Genetics. 130:1267-1276. doi: 10.1007/s00122-017-2886-4.
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, it is not known if both Tsn1 and Tsc1 are equally important in causing tan spot susceptibility. In this research, wheat lines were evaluated for reaction to various strains of the tan spot pathogen to determine the levels of susceptibility caused by each gene. Genetic analysis indicated that the effects of Tsn1 and Tsc1 were almost equal, and their effects contributed additively to tan spot susceptibility. These results indicate that wheat breeders should remove both genes from wheat lines to obtain good levels of tan spot resistance.
Technical Abstract: Tan spot of wheat, caused by Pyrenophora tritici-repentis, is an important disease in almost all wheat-growing areas of the world. The disease system is known to involve at least three fungal-produced necrotrophic effectors (NEs) that interact with corresponding host sensitivity (S) genes in an inverse gene-for-gene manner to induce disease. However, it is unknown if the effects of these NE-S gene interactions contribute additively to the development of tan spot. In this work, we conducted disease evaluations using different races and quantitative trait loci (QTL) analysis in a wheat recombinant inbred line (RIL) population derived from a cross between two susceptible genotypes, LMPG-6 and PI 626573. The two parental lines each harbored a single known NE sensitivity gene with LMPG-6 having the Ptr ToxC sensitivity gene Tsc1 and PI 626573 having the Ptr ToxA sensitivity gene Tsn1. Transgressive segregation was observed in the population for all races. QTL mapping revealed both loci (Tsn1 and Tsc1) were significantly associated with susceptibility to race 1 isolates, which produce both Ptr ToxA and Ptr ToxC, and the two genes contributed additively to tan spot susceptibility. For isolates of races 2 and 3, which produce only Ptr ToxA and Ptr ToxC, only Tsn1 and Tsc1 were associated with tan spot susceptibility, respectively. This work clearly demonstrates that tan spot susceptibility in this population is due primarily to two NE-S interactions. Breeders should remove both sensitivity genes from wheat lines to obtain high levels of tan spot resistance.