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ARS Home » Plains Area » Fargo, North Dakota » Edward T. Schafer Agricultural Research Center » Cereal Crops Research » Research » Publications at this Location » Publication #371191

Research Project: Improvement of Biotic Stress Resistance in Durum and Hard Red Spring Wheat Using Genetics and Genomics

Location: Cereal Crops Research

Title: Using forward and reverse genetics to clone the septoria nodorum blotch susceptibility gene Snn5 in wheat

item RUNNING, KATHERINE - North Dakota State University
item SHARMA, SAPNA - North Dakota State University
item Xu, Steven
item Friesen, Timothy
item Faris, Justin

Submitted to: Plant and Animal Genome Conference
Publication Type: Abstract Only
Publication Acceptance Date: 1/11/2020
Publication Date: 1/13/2020
Citation: Running, K., Sharma, S., Xu, S.S., Friesen, T.L., Faris, J.D. 2020. Using forward and reverse genetics to clone the septoria nodorum blotch susceptibility gene Snn5 in wheat [abstract]. Plant and Animal Genome Conference XXVIII. PO0945.

Interpretive Summary:

Technical Abstract: Parastagonospora nodorum is a necrotrophic fungal pathogen that causes the disease Septoria nodorum blotch (SNB). SNB reduces yield by decreasing the photosynthetic area of the plant. Wheat lines containing the Snn5 gene are sensitive to the P. nodorum-produced necrotrophic effector (NE) SnTox5, and a compatible Snn5-SnTox5 interaction plays a significant role in the development of SNB. The Snn5 locus was previously mapped to the long arm of chromosome 4B using a doubled haploid (DH) population derived from the T. turgidum ssp. carthlicum accession PI 94749 and the durum variety Lebsock. Here, we used the same population to conduct saturation mapping and delineate Snn5 to 2.8 cM, which corresponded to a 1.38 Mb interval containing 18 high-confidence genes in the Chinese Spring reference genome. Chinese Spring and Cadenza were both sensitive to SnTox5 and therefore carry functional alleles of Snn5. Both lines also harbored two genes within the Snn5 candidate region that both had similarity to the SnTox3 sensitivity gene Snn3-D1, which was cloned in a parallel project. Markers for the two genes cosegregated with Snn5, and analysis of Cadenza TILLING mutants for both genes revealed that one of the genes, but not the other, conditioned SnTox5 sensitivity. Comparative sequence analysis of additional EMS-induced SnTox5-insensitive mutants in the line LP29, which is a SnTox5 sensitive line from the DH population, further confirmed the candidate gene as Snn5. Work is ongoing to further characterize the structure, function, and origin of the Snn5 gene.