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ARS Home » Midwest Area » Ames, Iowa » Corn Insects and Crop Genetics Research » Research » Publications at this Location » Publication #386788
Research Project: Host and Pathogen Signaling in Cereal-Fungal Interactions

Location: Corn Insects and Crop Genetics Research

Title: Disruption of barley immunity to powdery mildew by an in-frame Lys-Leu deletion in the essential protein SGT1

Author
item CHAPMAN, ANTONY V - Iowa State University
item HUNT, MATTHEW - Iowa State University
item SURANA, PRIYANKA - Iowa State University
item VELASQUEZ-ZAPATA, VALERIA - Iowa State University
item XU, WEIHUI - Iowa State University
item Fuerst, Gregory
item Wise, Roger

Submitted to: Meeting Proceedings
Publication Type: Proceedings
Publication Acceptance Date: 6/7/2021
Publication Date: 12/8/2021
Citation: Chapman, A.E., Hunt, M., Surana, P., Velasquez-Zapata, V., Xu, W., Fuerst, G.S., Wise, R.P. 2021. Disruption of barley immunity to powdery mildew by an in-frame Lys-Leu deletion in the essential protein SGT1. Meeting Proceedings. 34. https://doi.org/10.1094/MPMI-34-7-S1.1.
DOI: https://doi.org/10.1094/MPMI-34-7-S1.1

Interpretive Summary:

Technical Abstract: Barley Mla (Mildew resistance locus a) and its nucleotide-binding, leucine-rich-repeat receptor (NLR) orthologs protect cereal grains from diseases caused by fungal pathogens. Yet, many intricacies of MLA protein-protein interactions and their effect on MLA-associated recognition remain unknown. To further characterize the molecular interactions required for NLR-based immunity, we used fast-neutron mutagenesis to screen 34,800 M2 families for plants compromised in MLA-mediated response to the powdery mildew fungus, Blumeria graminis f. sp. hordei. One variant, m11526, contained a novel mutation, designated rar3 (required for Mla6 resistance3), that abolishes race-specific resistance conditioned by the Mla6, Mla7 and Mla12 alleles, but does not compromise immunity mediated by Mla1, Mla9, Mla10 and Mla13. We used bulked-segregant-exome capture and fine mapping to delineate the causal mutation to an in-frame Lys-Leu deletion within the SGS domain of SGT1 (Suppressor of G-two allele of Skp1, Sgt1'KL308-309), the structural region that interacts with MLA proteins. In nature, mutations to Sgt1 are usually lethal, but we pinpoint a unique modification that delineates its requirement for some disease resistances, while unaffecting others as well as normal cell processes. Further study could distinguish the regions by which pathogen effectors and host proteins interact with SGT1, facilitating precise editing of effector-incompatible variants.