Skip to main content
ARS Home » Plains Area » Fargo, North Dakota » Edward T. Schafer Agricultural Research Center » Cereal Crops Research » Research » Publications at this Location » Publication #296420

Title: Identification and characterization of the SnTox6-Snn6 interaction in the Parastagonospora nodorum-wheat pathosystem

Author
item GAO, YUANYUAN - North Dakota State University
item Faris, Justin
item LIU, ZHAOHUI - North Dakota State University
item KIM, Y - North Dakota State University
item SYME, R - Curtin University
item OLIVER, R - Curtin University
item Xu, Steven
item Friesen, Timothy

Submitted to: Molecular Plant-Microbe Interactions
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/15/2015
Publication Date: 5/1/2015
Publication URL: http://handle.nal.usda.gov/10113/61003
Citation: Gao, Y., Faris, J.D., Liu, Z., Kim, Y.M., Syme, R.A., Oliver, R.P., Xu, S.S., Friesen, T.L. 2015. Identification and characterization of the SnTox6-Snn6 interaction in the Parastagonospora nodorum-wheat pathosystem. Molecular Plant-Microbe Interactions. 28(5):615-625.

Interpretive Summary: Stagonospora nodorum blotch (SNB) is a destructive disease in most wheat growing regions of the world. S. nodorum, causal agent of SNB, produces necrotrophic effectors (NEs) (Synonym=host selective toxin) that trigger disease development. The NE-host interaction is critical to inducing effector-triggered susceptibility. Currently, seven NE-host sensitivity gene interactions have been identified in the S. nodorum-wheat pathosystem. Here we report the characterization of the SnTox6-Snn6 interaction. SnTox6 is a novel proteinaceous NE that induces necrosis on sensitive wheat lines. A single gene in wheat designated Snn6 confers sensitivity to SnTox6 which we mapped to the long arm of chromosome 6A. The SnTox6-Snn6 interaction is light dependent, and accounted for 27% of the variation in SNB disease development in a segregating hexaploid wheat population. These findings expands our knowledge of the SNB interaction as well as providing information to breeding programs selecting for SNB resistance.

Technical Abstract: Stagonospora nodorum (teleomorph; Phaeosphaeria nodorum), is a necrotrophic filamentous fungal pathogen that causes Stagonospora nodorum blotch (SNB) on wheat. S. nodorum produces necrotrophic effectors (NE) that are recognized by dominant host sensitivity gene products resulting in disease development. The NE-host sensitivity gene interaction is critical to inducing effector-triggered susceptibility. Currently, seven NE-host sensitivity gene interactions have been identified in the S. nodorum-wheat pathosystem and each of them follows an inverse gene-for-gene model resulting in effector triggered susceptibility. Here we use the ITMI wheat mapping population, which we have previously shown to segregate for sensitivity to SnTox1 (Snn1) and SnTox3 (Snn3-B1) to show for the first time the identification of the novel NE SnTox6, the identification and mapping of Snn6 the corresponding wheat sensitivity gene, and the characterization of the significance of the SnTox6-Snn6 interaction. SnTox6 is a novel proteinaceous NE with an estimated size of 5-12 kDa that induces necrosis on wheat lines harboring Snn6. Snn6 confers sensitivity to SnTox6 and resides at the distal end of the long arm of wheat chromosome 6A. The SnTox6-Snn6 interaction was light dependent, and accounted for 27% of the variation in SNB disease development in the ITMI population. Interestingly, no other significant QTL were identified even though the S. nodorum isolate used in this study (Sn6) harbors both the SnTox1 and SnTox3 genes. RT-PCR showed that SnTox3 was expressed at high levels 72 h post inoculation; however, SnTox1 was not expressed at the same time point, the time point previously shown to be the peak of SnTox1 and SnTox3 in planta expression, showing that gene regulation of necrotrophic effectors is isolate specific. This work expands our knowledge of the wheat-S. nodorum interaction and further establishes this system as a model for other host-necrotroph pathosystems.