Location: National Peanut Research Laboratory
Title: Characterizing phenotype variants of cercosporidium personatum, causal agent of peanut late leaf spot disease, their morphology, genetics and metabolitesAuthor
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Arias De Ares, Renee |
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CANTONWINE, EMILY - Valdosta State University |
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Orner, Valerie |
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Walk, Travis |
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Massa, Alicia |
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STEWART, JANE - Colorado State University |
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DOBBS, JOHN - Colorado State University |
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MANCHESTER, ATALAYA - Valdosta State University |
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Higbee, Pirada |
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Lamb, Marshall |
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Sobolev, Victor |
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Submitted to: Scientific Reports
Publication Type: Peer Reviewed Journal Publication Acceptance Date: 1/7/2025 Publication Date: 1/9/2025 Citation: Arias De Ares, R.S., Cantonwine, E., Orner, V.A., Walk, T., Massa, A.N., Stewart, J., Dobbs, J., Manchester, A., Higbee, P.S., Lamb, M.C., Sobolev, V. 2025. Characterizing phenotype variants of cercosporidium personatum, causal agent of peanut late leaf spot disease, their morphology, genetics and metabolites. Scientific Reports. 15, 1405. https://doi.org/10.1038/s41598-025-85953-9. DOI: https://doi.org/10.1038/s41598-025-85953-9 Interpretive Summary: The long term disease resistance of plants depends on how fast the pathogens can evolve to overcome the plant defenses, the evolution of that ability is directly related to the genetic variation and reproductive biology of the pathogen. Analyzing these two factors is particularly difficult in the fungi that cause early and late leaf spot (ELS and LLS) disease in peanut, as they grow extremely slow in culture (about 4 mm in 6 months). Here, we analyzed the genetic variation of four distinct isolates of the LLS pathogen, their genetic expression, their chemical profiles (including melanin, chitin and multiple genotoxic compounds), and describe in detail two mating types of this fungal species, as well as a method for the fast (only 5 days) evaluation of fungicide resistance which was not feasible before. Technical Abstract: Cercosporidium personatum (CP) causes peanut late leaf spot (LLS) disease with 70% yield losses unless controlled by fungicides. CP grows slowly in culture, exhibiting variable phenotypes. To explain those variations, we analyzed the morphology, genomes, transcriptomes and chemical composition of three morphotypes, herein called RED, TAN, and BROWN. We characterized, for the first time in CP, anthraquinone (AQ) precursors of dothistromin (DOT), including averantin, averufin, norsolorinic acid, versicolorin B, versicolorin A, nidurufin and averufanin. BROWN had the highest AQ and melanin (15 mg/g DW) contents. RED had the highest ergosterol (855 µM FW) and chitin (beta-glucans, 4% DW) contents. RED and TAN had higher resistance to xenobiotics (p'='1.0E-3), including chlorothalonil, tebuconazole and caffeine, compared to CP NRRL 64463. In RED, TAN, and BROWN, rates of single nucleotide polymorphisms (SNP) (1.4–1.7 nt/kb) and amino acid changes (3k-4k) were higher than in NRRL 64463. Differential gene expression (p'='1.0E-5) was observed in 47 pathogenicity/virulence genes, 41 carbohydrate-active enzymes (CAZymes), and 23 pigment/mycotoxin biosynthesis genes. We describe the MAT1 locus, and a method to evaluate CP-xenobiotic resistance in 5 days. Chemical profiles indicate each CP morphotype could trigger different immune response in plants, probably hindering development of durable LLS resistance. |
