Association mapping reveals a reciprocal virulence/avirulence locus within diverse US Pyrenophora teres f. maculata isolates

Authors: CLARE, SHAUN - Washington State University; DUELLMAN, KASIA - Washington State University; RICHARDS, JONATHAN - Louisiana State University Agcenter; POUDEL, ROSHAN - North Dakota State University; MERRICK, LANCE - Washington State University; Friesen, Timothy; BRUEGGEMAN, ROBERT - Washington State University

Submitted to: BMC Genomics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/17/2022
Publication Date: 4/9/2022
Citation: Clare, S., Duellman, K., Richards, J., Poudel, R., Merrick, L., Friesen, T.L., Brueggeman, R.S. 2022. Association mapping reveals a reciprocal virulence/avirulence locus within diverse US Pyrenophora teres f. maculata isolates. BMC Genomics. 23. Article 285. https://doi.org/10.1186/s12864-022-08529-1.
DOI: https://doi.org/10.1186/s12864-022-08529-1

Interpretive Summary: Outbreaks of spot form net blotch of barley have recently resulted in major yield and quality losses for growers in several areas of the world, including the Northern Great Plains of the United States. How the causal fungal pathogen is infecting and causing disease is poorly understood and understanding of the infection processes is necessary for controlling the pathogen through host resistance and/or cultural practices. Pathogen isolates collected from North Dakota, Montana, and Idaho were used to identify the location of virulence genes that induce disease on barley. Several genetic loci were identified that can now be mined for genes that are contributing to the induction of spot form net blotch disease symptoms. This work is important to barley pathologists and barley breeders working toward controlling spot form net blotch of barley.

Technical Abstract: Background Spot form net blotch (SFNB) caused by the necrotrophic fungal pathogen Pyrenophora teres f. maculata (Ptm) is an economically important disease of barley that also infects wheat. Using genetic analysis to characterize loci in Ptm genomes associated with virulence or avirulence is an important step to identify pathogen effectors that determine compatible (virulent) or incompatible (avirulent) interactions with cereal hosts. Association mapping (AM) is a powerful tool for detecting virulence loci utilizing phenotyping and genotyping data generated for natural populations of plant pathogenic fungi. Results Restriction-site associated DNA genotyping-by-sequencing (RAD-GBS) was used to generate 4,836 single nucleotide polymorphism (SNP) markers for a natural population of 103 Ptm isolates collected from Idaho, Montana and North Dakota. Association mapping analyses were performed utilizing the genotyping and infection type data generated for each isolate when challenged on barley seedlings of thirty SFNB differential barley lines. A total of 39 marker trait associations (MTAs) were detected across the 20 barley lines corresponding to 30 QTL; 26 novel QTL and 4 that were previously mapped in Ptm biparental populations. These results using diverse US isolates and barley genotypes showed numerous barley-Ptm genetic interactions with 7 of the 30 Ptm virulence/avirulence loci falling on chromosome 3 suggesting that it is a reservoir of diverse virulence effectors. One of the loci exhibited reciprocal virulence/avirulence with one haplotype predominantly present in isolates collected from Idaho increasing susceptibility in barley line MXB468 and the alternative haplotype predominantly present in isolates collected from North Dakota and Montana increasing susceptibility in barley line CI9819. Conclusions Association mapping provided novel insight into the host pathogen genetic interactions occurring in the barley-Ptm pathosystem. The analysis suggests that chromosome 3 of Ptm serves as an effector reservoir in concordance with previous reports for Pyrenophora teres f. teres the causal agent of the closely related disease net form net blotch. Additionally, these analyses identified the first reported case of a reciprocal pathogen virulence locus. However, further investigation of the pathosystem is required to determine if multiple genes or alleles of the same gene are responsible for this genetic phenomenon.