Location: Cereal Crops Improvement Research
Project Number: 3060-22000-051-012-S
Project Type: Non-Assistance Cooperative Agreement
Start Date: Jun 1, 2026
End Date: Dec 31, 2027
Objective:
The objectives of this cooperative research project are to:
1) Characterize the mode of action of the effector SnTox267 from Parastagonospora nodorum
2) Functionally validate and characterize the v5791 gene from Pyrenophora teres f. teres
Approach:
Fungal diseases of cereals cause major global losses through reduced yield, lower grain quality, and increased inputs such as fungicides. Parastagonospora nodorum is an important wheat pathogen that infects leaves and glumes, reducing yield. This necrotrophic interaction relies on pathogen exploitation of host pathways, yet necrotroph attachment and colonization mechanisms remain far less understood than those of biotrophs.Our work shows that P. nodorum deploys multiple necrotrophic effectors (NEs) that target host susceptibility pathways, inducing cell death and releasing nutrients. However, the molecular mechanisms behind NE activity and the pathogen’s strategies to evade or suppress defenses such as oxidative bursts, antimicrobial compounds, and pathogenesis-related proteins remain poorly defined.We have identified several classical effector candidates that may manipulate or circumvent host defenses. Their characterization, along with the known effector SnTox267, will include heterologous protein expression, subcellular localization, CRISPR-Cas9 editing, fungal transformation, yeast two-hybrid assays, and confocal microscopy. Effector gene disruptions will validate candidate functions.This work will clarify how P. nodorum manipulates wheat to establish infection, supporting improved management strategies for necrotrophic diseases.Pyrenophora teres f. teres, the causal agent of net form net blotch (NFNB), is one of the most damaging barley pathogens worldwide. Losses arise from reduced yield, decreased grain quality, and increased fungicide use. As a necrotroph, it relies on host cell death, yet key mechanisms of infection, host manipulation, and adaptation to resistant barley genotypes remain unclear.Evidence indicates that P. teres f. teres uses diverse effectors to exploit susceptibility loci or disrupt resistance pathways. However, effector activity, host recognition, and defense suppression mechanisms remain largely uncharacterized. Our research focuses on identifying and characterizing effectors involved in both susceptibility targeting and resistance circumvention.The effector gene v5791 enables the pathogen to suppress or bypass Rpt5, a widely effective barley resistance source. This project will validate and characterize v5791, analyze its protein function, and identify host targets via yeast two-hybrid assays.The knowledge gained will improve understanding of how P. teres f. teres manipulates barley defenses to colonize tissue and reproduce, ultimately supporting better strategies for managing NFNB and other necrotrophic diseases.