Location: Cereal Crops ResearchTitle: New insights into the roles of host gene-necrotrophic effector interactions in governing susceptibility of durum wheat to tan spot and Septoria nodorum blotch Author
|Virdi, Simerjot - North Dakota State University|
|Liu, Zhaohui - North Dakota State University|
Submitted to: Genes, Genomes, Genetics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/31/2016
Publication Date: 12/1/2016
Citation: Virdi, S.K., Liu, Z., Overlander, M., Zhang, Z., Xu, S.S., Friesen, T.L., Faris, J.D. 2016. New insights into the roles of host gene-necrotrophic effector interactions in governing susceptibility of durum wheat to tan spot and Septoria nodorum blotch. Genes, Genomes, Genetics. 6:4139-4150. doi: 10.1534/g3.116.036525.
Interpretive Summary: Tan spot and Septoria nodorum blotch (SNB) are diseases of both common and durum wheat. The effects of molecular host-pathogen interactions known to govern susceptibility of common wheat to these diseases have not been well studied in durum wheat. Here, research indicated that one interaction conditions susceptibility to tan spot in both common and durum wheat. However, a second interaction known to govern susceptibility to both tan spot and SNB in common wheat was only associated with the development of SNB in durum wheat, indicating that other factors are involved in tan spot susceptibility of durum wheat.
Technical Abstract: Tan spot and Septoria nodorum blotch (SNB) are important diseases of wheat caused by the necrotrophic fungi Pyrenophora tritici-repentis and Parastagonospora nodorum, respectively. The P. tritici-repentis necrotrophic effector (NE) Ptr ToxB causes tan spot when recognized by the Tsc2 gene. The NE ToxA is produced by both pathogens and has been associated with the development of both tan spot and SNB when recognized by the wheat Tsn1 gene. Most work to study these interactions has been conducted in common wheat, but little has been done in durum wheat. Here, analysis indicated that the Tsc2-Ptr ToxB interaction plays a prominent role in the development of tan spot in durum. However, the Tsn1-ToxA interaction was not associated with the development of tan spot, but was strongly associated with the development of SNB. Parastagonospora nodorum expressed ToxA at high levels in infected Tsn1 plants, whereas ToxA expression in P. tritici-repentis was barely detectable, suggesting that the differences in disease levels associated with the Tsn1-ToxA interaction were due to differences in pathogen expression of ToxA. These and previous results together indicate that: 1) the effects of Tsn1-ToxA on tan spot in common wheat can range from nonsignificant to highly significant depending on the host genetic background; 2) Tsn1-ToxA is not a significant factor for tan spot development in durum wheat; and 3) Tsn1-ToxA plays a major role in SNB development in both common and durum wheat. Durum and common wheat breeders alike should strive to remove both Tsc2 and Tsn1 from their materials to achieve disease resistance.