|LIU, ZHAOHUI - North Dakota State University|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 9/14/2016
Publication Date: 11/2/2016
Citation: Faris, J.D., Friesen, T.L., Liu, Z., Xu, S.S. 2016. Unraveling the genetics of wheat-necrotrophic pathogen interactions reveals a conundrum [abstract]. Durable Wheat Resistance Meeting, November 2-3, 2016, Minneapolis, MN.
Technical Abstract: Interactions between wheat and the necrotrophic pathogens Parastagonospora nodorum (Pn) and Pyrenophora tritici-repentis (Ptr), which cause the foliar diseases Septoria nodorum blotch (SNB) and tan spot, respectively, involve host genes that recognize pathogen-produced necrotrophic effectors (NEs) in an inverse gene-for-gene manner to cause disease. Over the past decade, we have identified and characterized numerous host gene-NE interaction pairs, and we have cloned two wheat NE sensitivity genes, namely Tsn1 and Snn1. Tsn1, which confers sensitivity to ToxA produced by both Ptr and Pn, is a member of the NB-LRR class of disease resistance-like genes. Snn1 recognizes the Pn NE SnTox1 and is a wall-associated kinase, which are known to serve as pathogen recognition receptors associated with disease resistance. These results suggest necrotrophic specialists such as Ptr and Pn use NEs to exploit pathways often associated with resistance to biotrophs. So far, it appears that genetic variation in the wheat-Pn system mostly involves host gene-NE interactions (nine have been identified), but the situation in the wheat-Ptr system is more complex. Whereas the Tsn1-ToxA interaction is consistently associated with disease in the wheat-Pn system, it is background-dependent in the wheat-Ptr system. We have also identified a major dominant race-nonspecific tan spot resistance gene on wheat chromosome arm 3BL. Therefore, both resistance and susceptibility genes are likely involved in the wheat-Ptr system. This work has shed light on the mechanisms associated with necrotrophic effector triggered susceptibility, but has also revealed that breeders may face a conundrum in that introgression of biotroph resistance genes may concomitantly introduce necrotroph susceptibility genes.