jasmonic-acid and indole

Herbivore-induced plant volatiles prime plant defenses and resistance, but how they are integrated into early defense signaling and whether a causal relationship exists between volatile defense priming and herbivore resistance is unclear. Here, we investigated the impact of indole, a common herbivore-induced plant volatile and modulator of many physiological processes in plants, bacteria, and animals, on early defense signaling and herbivore resistance in rice (

Topics: Animals; Cyclopentanes; Disease Resistance; Gene Expression Regulation, Plant; Herbivory; Indoles; Mitogen-Activated Protein Kinases; Oryza; Oxylipins; Plant Diseases; Plant Growth Regulators; Plant Proteins; Plants, Genetically Modified; Signal Transduction; Spodoptera

Herbivore-induced volatile organic compounds prime non-attacked plant tissues to respond more strongly to subsequent attacks. However, the key volatiles that trigger this primed state remain largely unidentified. In maize, the release of the aromatic compound indole is herbivore-specific and occurs earlier than other induced responses. We therefore hypothesized that indole may be involved in airborne priming. Using indole-deficient mutants and synthetic indole dispensers, we show that herbivore-induced indole enhances the induction of defensive volatiles in neighbouring maize plants in a species-specific manner. Furthermore, the release of indole is essential for priming of mono- and homoterpenes in systemic leaves of attacked plants. Indole exposure markedly increases the herbivore-induced production of the stress hormones jasmonate-isoleucine conjugate and abscisic acid, which represents a likely mechanism for indole-dependent priming. These results demonstrate that indole functions as a rapid and potent aerial priming agent that prepares systemic tissues and neighbouring plants for incoming attacks.

Topics: Abscisic Acid; Animals; Cyclopentanes; Herbivory; Indoles; Mutation; Oxylipins; Plant Growth Regulators; Terpenes; Volatile Organic Compounds; Zea mays

Simultaneous mutation of two WRKY-type transcription factors, WRKY18 and WRKY40, renders otherwise susceptible wild-type Arabidopsis plants resistant towards the biotrophic powdery mildew fungus Golovinomyces orontii. Resistance in wrky18 wrky40 double mutant plants is accompanied by massive transcriptional reprogramming, imbalance in salicylic acid (SA) and jasmonic acid (JA) signaling, altered ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) expression, and accumulation of the phytoalexin camalexin. Genetic analyses identified SA biosynthesis and EDS1 signaling as well as biosynthesis of the indole-glucosinolate 4MI3G as essential components required for loss-of-WRKY18 WRKY40-mediated resistance towards G. orontii. The analysis of wrky18 wrky40 pad3 mutant plants impaired in camalexin biosynthesis revealed an uncoupling of pre- from postinvasive resistance against G. orontii. Comprehensive infection studies demonstrated the specificity of wrky18 wrky40-mediated G. orontii resistance. Interestingly, WRKY18 and WRKY40 act as positive regulators in effector-triggered immunity, as the wrky18 wrky40 double mutant was found to be strongly susceptible towards the bacterial pathogen Pseudomonas syringae DC3000 expressing the effector AvrRPS4 but not against other tested Pseudomonas strains. We hypothesize that G. orontii depends on the function of WRKY18 and WRKY40 to successfully infect Arabidopsis wild-type plants while, in the interaction with P. syringae AvrRPS4, they are required to mediate effector-triggered immunity.

Topics: Arabidopsis; Arabidopsis Proteins; Ascomycota; Botrytis; Cyclopentanes; Disease Resistance; DNA-Binding Proteins; Gene Expression Regulation, Plant; Glucosinolates; Indoles; Mutation; Oomycetes; Oxylipins; Plant Diseases; Plant Growth Regulators; Plant Leaves; Plants, Genetically Modified; Pseudomonas syringae; Salicylic Acid; Signal Transduction; Thiazoles; Transcription Factors

The phytotoxin coronatine (COR) promotes various aspects of Pseudomonas syringae virulence, including invasion through stomata, growth in the apoplast, and induction of disease symptoms. COR is a structural mimic of active jasmonic acid (JA) conjugates. Known activities of COR are mediated through its binding to the F-box-containing JA coreceptor CORONATINE INSENSITIVE1. By analyzing the interaction of P. syringae mutants with Arabidopsis thaliana mutants, we demonstrate that, in the apoplastic space of Arabidopsis, COR is a multifunctional defense suppressor. COR and the critical P. syringae type III effector HopM1 target distinct signaling steps to suppress callose deposition. In addition to its well-documented ability to suppress salicylic acid (SA) signaling, COR suppresses an SA-independent pathway contributing to callose deposition by reducing accumulation of an indole glucosinolate upstream of the activity of the PEN2 myrosinase. COR also suppresses callose deposition and promotes bacterial growth in coi1 mutant plants, indicating that COR may have multiple targets inside plant cells.

Topics: Amino Acids; Arabidopsis; Arabidopsis Proteins; Cyclopentanes; Gene Expression Regulation, Plant; Glucans; Glucosinolates; Host-Pathogen Interactions; Indenes; Indoles; Mutation; N-Glycosyl Hydrolases; Oxylipins; Plant Diseases; Plant Growth Regulators; Plant Immunity; Pseudomonas syringae; Salicylic Acid; Signal Transduction; Virulence

ZmPep1 is a bioactive peptide encoded by a previously uncharacterized maize (Zea mays) gene, ZmPROPEP1. ZmPROPEP1 was identified by sequence similarity as an ortholog of the Arabidopsis (Arabidopsis thaliana) AtPROPEP1 gene, which encodes the precursor protein of elicitor peptide 1 (AtPep1). Together with its receptors, AtPEPR1 and AtPEPR2, AtPep1 functions to activate and amplify innate immune responses in Arabidopsis and enhances resistance to both Pythium irregulare and Pseudomonas syringae. Candidate orthologs to the AtPROPEP1 gene have been identified from a variety of crop species; however, prior to this study, activities of the respective peptides encoded by these orthologs were unknown. Expression of the ZmPROPEP1 gene is induced by fungal infection and treatment with jasmonic acid or ZmPep1. ZmPep1 activates de novo synthesis of the hormones jasmonic acid and ethylene and induces the expression of genes encoding the defense proteins endochitinase A, PR-4, PRms, and SerPIN. ZmPep1 also stimulates the expression of Benzoxazineless1, a gene required for the biosynthesis of benzoxazinoid defenses, and the accumulation of 2-hydroxy-4,7-dimethoxy-1,4-benzoxazin-3-one glucoside in leaves. To ascertain whether ZmPep1-induced defenses affect resistance, maize plants were pretreated with the peptide prior to infection with fungal pathogens. Based on cell death and lesion severity, ZmPep1 pretreatment was found to enhance resistance to both southern leaf blight and anthracnose stalk rot caused by Cochliobolis heterostrophus and Colletotrichum graminicola, respectively. We present evidence that peptides belonging to the Pep family have a conserved function across plant species as endogenous regulators of innate immunity and may have potential for enhancing disease resistance in crops.

Topics: Amino Acid Sequence; Arabidopsis; Ascomycota; Benzoxazines; Colletotrichum; Cyclopentanes; Ethylenes; Gene Expression Regulation, Plant; Genes, Plant; Immunity, Innate; Indoles; Molecular Sequence Data; ortho-Aminobenzoates; Oxylipins; Peptides; Plant Diseases; Plant Proteins; Sequence Homology, Amino Acid; Signal Transduction; Transcription, Genetic; Zea mays

Jasmonic acid (JA) is a fatty acid-derived signaling molecule that regulates a broad range of plant defense responses against herbivores and some microbial pathogens. Molecular genetic studies have established that JA also performs a critical role in several aspects of plant development. Here, we describe the characterization of the Arabidopsis mutant jasmonic acid-hypersensitive1-1 (jah1-1), which is defective in several aspects of JA responses. Although the mutant exhibits increased sensitivity to JA in root growth inhibition, it shows decreased expression of JA-inducible defense genes and reduced resistance to the necrotrophic fungus Botrytis cinerea . Gene cloning studies indicate that these defects are caused by a mutation in the cytochrome P450 protein CYP82C2. We provide evidence showing that the compromised resistance of the jah1-1 mutant to B . cinerea is accompanied by decreased expression of JA-induced defense genes and reduced accumulation of JA-induced indole glucosinolates (IGs). Conversely, the enhanced resistance to B. cinerea in CYP82C2-overexpressing plants is accompanied by increased expression of JA-induced defense genes and elevated levels of JA-induced IGs. We demonstrate that CYP82C2 affects JA-induced accumulation of the IG biosynthetic precursor tryptophan (Trp), but not the JA-induced IAA or pathogen-induced camalexin. Together, our results support a hypothesis that CYP82C2 may act in the metabolism of Trp-derived secondary metabolites under conditions in which JA levels are elevated. The jah1-1 mutant should thus be important in future studies toward understanding the mechanisms underlying the complexity of JA-mediated differential responses, which are important for plants to adapt their growth to the ever-changing environments.

Topics: Arabidopsis; Arabidopsis Proteins; Botrytis; Cyclopentanes; Cytochrome P-450 Enzyme System; Gene Expression Regulation, Plant; Genes, Plant; Glucosinolates; Indoles; Mutation; Oxylipins; Plant Diseases; Plant Roots

Jasmonic acid (JA) has long been hypothesized to be an important regulator of insect-induced volatile emission; however, current models are based primarily on circumstantial evidence derived from pharmacological studies. Using beet armyworm caterpillars (BAW: Spodoptera exigua) and intact corn seedlings, we examine this hypothesis by measuring both the time-course of insect-induced JA levels and the relationships between endogenous JA levels, ethylene, indole and sesquiterpenes. In separate Morning and Evening time-course trials, BAW feeding stimulated increases in JA levels within the first 4-6 h and resulted in maximal increases in JA, indole, sesquiterpenes and ethylene 8-16 h later. During BAW herbivory, increases in JA either paralleled or preceded the increases in indole, sesquiterpenes and ethylene in the Morning and Evening trials, respectively. By varying the intensity of the BAW herbivory, we demonstrate that strong positive relationships exist between the resulting variation in insect-induced JA levels and volatile emissions such as indole and the sesquiterpenes. To address potential signaling interactions between herbivore-induced JA and ethylene, plants were pretreated with 1-methylcyclopropene (1-MCP), an inhibitor of ethylene perception. 1-MCP pretreatment resulted in reduced production of ethylene and volatile emission following BAW herbivory but did not alter the insect-induced accumulation of JA. Our results strongly support a role for JA in the regulation of insect-induced volatile emission but also suggest that ethylene perception regulates the magnitude of volatile emission during herbivory.

Topics: Animals; Cyclopentanes; Cyclopropanes; Ethylenes; Host-Parasite Interactions; Indoles; Larva; Oxylipins; Plant Diseases; Sesquiterpenes; Signal Transduction; Spodoptera; Volatilization; Zea mays