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ARS Home » Southeast Area » Gainesville, Florida » Center for Medical, Agricultural and Veterinary Entomology » Chemistry Research » Research » Publications at this Location » Publication #375792

Research Project: Molecular and Biochemical Characterization of Biotic and Abiotic Stress on Plant Defense Responses in Maize

Location: Chemistry Research

Title: Green Leaf volatiles and jasmonic acid enhance susceptibility to anthracnose diseases caused by Colletotrichum graminicola in maize

Author
item GORMAN, ZACHARY - Texas A&M University
item Christensen, Shawn
item YAN, YUANXIN - Nanjing University
item YE, YONGMING - Nanchang University
item BORREGO, ELI - Rochester Institute Of Technology
item KOLOMIETS, MICHAEL - Texas A&M University

Submitted to: Molecular Plant Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/29/2020
Publication Date: 5/1/2020
Citation: Gorman, Z., Christensen, S.A., Yan, Y., Ye, Y., Borrego, E., Kolomiets, M.V. 2020. Green Leaf volatiles and jasmonic acid enhance susceptibility to anthracnose diseases caused by Colletotrichum graminicola in maize. Molecular Plant Pathology. 21(5):702-715. https://doi.org/10.1111/mpp.12924.
DOI: https://doi.org/10.1111/mpp.12924

Interpretive Summary: Crop loss due to pathogen attack is a recurring global problem leading to billions of dollars in reduced yield and revenue annually. Contributing factors are two damaging diseases of maize called anthracnose leaf blight (ALB) and anthracnose stalk rot (ASR). Despite substantial economic losses caused by ASR and ALB, very limited knowledge exists about maize immune responses to these threats. ARS Scientists at the Center for Medical, Agricultural, and Veterinary Entomology in Gainesville, FL, in collaboration with researchers from Texas A&M University discovered that several molecular features normally involved in disease resistance were unexpectedly contributing to ASR and ALB susceptibility in maize. These features include odors emitted by the plant called green leaf volatiles (GLVs) and a plant hormone termed jasmonic acid (JA). Genetic alterations in the genes that produce GLVs and JA increased the plants’ resistance against ALB and ASR. This information provides breeders with important genetic information that may contribute to improved disease resistance in maize, thus alleviating large economic losses that corn growers experience due to these threats.

Technical Abstract: Colletotrichum graminicola is a hemibiotrophic fungus that causes anthracnose leaf blight (ALB) and anthracnose stalk rot (ASR) in maize. Despite substantial economic losses caused by these diseases, the defence mechanisms against this pathogen remain poorly understood. Several hormones are suggested to aid in defence against C. graminicola, such as jasmonic acid (JA) and salicylic acid (SA), but supporting genetic evidence was not reported. Green leaf volatiles (GLVs) are a group of well-characterized volatiles that induce JA biosynthesis in maize and are known to function in defence against necrotrophic pathogens. Information regarding the role of GLVs and JA in interactions with (hemi)biotrophic pathogens remains limited. To functionally elucidate GLVs and JA in defence against a hemibiotrophic pathogen, we tested GLV- and JA-deficient mutants, lox10 and opr7 opr8, respectively, for resistance to ASR and ALB and profiled jasmonates and SA in their stalks and leaves throughout infection. Both mutants were resistant and generally displayed elevated levels of SA and low amounts of jasmonates, especially at early stages of infection. Pretreatment with GLVs restored susceptibility of lox10 mutants, but not opr7 opr8 mutants, which coincided with complete rescue of JA levels. Exogenous methyl jasmonate restored susceptibility in both mutants when applied before inoculation, whereas methyl salicylate did not induce further resistance in either of the mutants, but did induce mutant-like resistance in the wild type. Collectively, this study reveals that GLVs and JA contribute to maize susceptibility to C. graminicola due to suppression of SA-related defences.