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ARS Home » Plains Area » Fargo, North Dakota » Edward T. Schafer Agricultural Research Center » Sunflower and Plant Biology Research » Research » Publications at this Location » Publication #337737

Research Project: Sunflower Genetic Improvement with Genes from Wild Crop Relatives and Domesticated Sunflower

Location: Sunflower and Plant Biology Research

Title: PMR5, an acetylation protein at the intersection of pectin biosynthesis and defense against fungal pathogens

Author
item CHINIQUY, DAWN - University Of California
item Underwood, William
item CORWIN, JASON - University Of California
item RYAN, ANDREW - University Of California
item SZEMENYEI, HEIDI - University Of California
item CHERK LIM, CANDICE - University Of California
item STONEBLOOM, SOLOMON - Joint Bioenergy Institute (JBEI)
item BIRDSEYE, DEVON - Joint Bioenergy Institute (JBEI)
item VOGEL, JOHN - Joint Genome Institute
item KLIEBENSTEIN, DANIEL - University Of California
item SCHELLER, HENRIK - Joint Bioenergy Institute (JBEI)
item SOMERVILLE, SHAUNA - University Of California

Submitted to: Plant Journal
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/17/2019
Publication Date: 8/14/2019
Citation: Chiniquy, D., Underwood, W., Corwin, J., Ryan, A., Szemenyei, H., Cherk Lim, C., Stonebloom, S.H., Birdseye, D.S., Vogel, J., Kliebenstein, D., Scheller, H.V., Somerville, S. 2019. PMR5, an acetylation protein at the intersection of pectin biosynthesis and defense against fungal pathogens. Plant Journal. 100(5):1022-1035. https://doi.org/10.1111/tpj.14497.
DOI: https://doi.org/10.1111/tpj.14497

Interpretive Summary: Powdery mildew fungi infect a large number of agriculturally and horticulturally important plant species, causing significant economic losses. The Arabidopsis pmr5 mutant displays resistance to normally pathogenic species of powdery mildew, such as Golovinomyces cichoracearum, and this resistance has previously been associated with altered cell wall composition of the mutant. However, the function of PMR5 and the link between altered cell wall composition and increased resistance to powdery mildew remained enigmatic. Here, we propose a role for PMR5 in acetylation of pectin cell wall polymers and provide further evidence for a complex interplay between cell wall composition and pathogen susceptibility.

Technical Abstract: Powdery mildew (Golovinomyces cichoracearum), one of the most prolific obligate biotrophic fungal pathogens worldwide, infects its host by penetrating the plant cell wall while avoiding the activation of the plant’s innate immune system. The Arabidopsis mutant powdery mildew resistant5 (pmr5) carries a mutation in a putative pectin acetyltransferase gene, which confers enhanced resistance to powdery mildew. Here, we show that heterologously expressed PMR5 protein transfers acetyl groups from [14C]- acetyl-CoA to oligogalacturonides. Through site-directed mutagenesis, we show that three amino acids within an esterase domain highly conserved in putative PMR5 orthologs that are necessary for PMR5 complementation. A suppressor screen of mutagenized pmr5 seed selected for return of powdery mildew susceptibility produced 20 mutant suppressors of G. cichoracearum disease resistance, two of these map to previously characterized genes affecting acetylation of plant cell wall polysaccharides, RWA2 and TBR. These two suppressors also suppress powdery mildew disease resistance in pmr6, an encoding a putative pectate lyase gene. Cell wall analysis of pmr5, pmr6, and their two cell wall suppressors, shows minor shifts in cellulose and pectin composition. Interestingly, both pmr5 and pmr6 plants exhibit increased susceptibility to multiple strains of the generalist necrotroph Botrytis cinerea and have decreased camalexin production upon B. cinerea infection. These findings illustrate the trade-offs between cell wall polysaccharide composition and fungal disease resistance, and outline a potential route for engineering powdery mildew resistance into susceptible crop species and also engineering biofuel crops for decreased inhibition by acetate during fermentation.