Location: Cereal Crops ResearchTitle: A tale of three wheat genes reveals the ability of a necrotrophic pathogen to bamboozle diverse host targets
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 5/16/2019
Publication Date: 7/21/2019
Citation: Faris, J.D., Zhang, Z., Friesen, T.L. 2019. A tale of three wheat genes reveals the ability of a necrotrophic pathogen to bamboozle diverse host targets [abstract]. 1st International Wheat Congress. July 21-26, 2019. Saskatoon, Saskatchewan, Canada. Abstract No. 019196.
Technical Abstract: Parastagonospora nodorum is a necrotrophic fungal pathogen of wheat that causes the disease septoria nodorum blotch (SNB). Genetic dissection of the wheat-P. nodorum pathosystem over the past two decades has led to the identification of nine specific inverse gene-for-gene interactions, where the recognition of pathogen-produced molecules known as necrotrophic effectors (NEs) by dominant host genes leads to a plant ‘defense’ response typical of that observed in classical R gene-Avr gene interactions. However, because the pathogen is a necrotroph, it can feed on dead tissue and ultimately propagate, thus leading to susceptibility as opposed to resistance. We previously reported the cloning of two of the nine wheat susceptibility genes, Tsn1 and Snn1, and we have now cloned a third gene, Snn3-D1. Tsn1 contains protein kinase (PK), nucleotide binding, and leucine-rich repeat domains and therefore resembles a classic resistance gene. Snn1 resembles a pathogen recognition receptor in that it is a wall-associated kinase with PK, transmembrane, galacturonan binding, and calcium binding domains. The cloning of Snn3-D1 revealed that it falls into neither of these classes, and although it harbors a PK domain, it harbors another domain essential for function that is rare among plant genes. Snn3-D1 also differs from Tsn1 and Snn1 in its light regulated and circadian expression patterns. This and other characteristics of Snn3-D1 and how it compares to Tsn1 and Snn1 will be presented. Overall, these results show that P. nodorum can hijack diverse classes of host genes to cause disease. However, one common feature of the three genes is the presence of a PK domain, which indicates that a signaling mechanism is likely necessary for the pathogen to exploit programmed cell death in the host.