Differential Induction of Plant Volatile Biosynthesis in the Lima Bean by Early and Late Intermediates of the Octadecanoid-Signaling Pathway

Plants are able to respond to herbivore damage with de novo biosynthesis of an herbivore-characteristic blend of volatiles. The signal transduction initiating volatile biosynthesis may involve the activation of the octadecanoid pathway, as exemplified by the transient increase of endogenous jasmonic acid (JA) in leaves of lima bean (Phaseolus lunatus) after treatment with the macromolecular elicitor cellulysin. Within this pathway lima bean possesses at least two different biologically active signals that trigger different biosynthetic activities. Early intermediates of the pathway, especially 12-oxo-phytodienoic acid (PDA), are able to induce the biosynthesis of the diterpenoid-derived 4,8,12-trimethyltrideca-1,3,7,11-tetraene. High concentrations of PDA result in more complex patterns of additional volatiles. JA, the last compound in the sequence, lacks the ability to induce diterpenoid-derived compounds, but is highly effective at triggering the biosynthesis of other volatiles. The phytotoxin coronatine and amino acid conjugates of linolenic acid (e.g. linolenoyl-l-glutamine) mimic the action of PDA, but coronatine does not increase the level of endogenous JA. The structural analog of coronatine, the isoleucine conjugate of 1-oxo-indanoyl-4-carboxylic acid, effectively mimics the action of JA, but does not increase the level of endogenous JA. The differential induction of volatiles resembles previous findings on signal transduction in mechanically stimulated tendrils of Bryonia dioica

Ion Channel-Forming Alamethicin Is a Potent Elicitor of Volatile Biosynthesis and Tendril Coiling. Cross Talk between Jasmonate and Salicylate Signaling in Lima Bean

Alamethicin (ALA), a voltage-gated, ion channel-forming peptide mixture from Trichoderma viride, is a potent elicitor of the biosynthesis of volatile compounds in lima bean (Phaseolus lunatus). Unlike elicitation with jasmonic acid or herbivore damage, the blend of substances emitted comprises only the two homoterpenes, 4,11-dimethylnona-1,3,7-triene and 4,8,12-trimethyltrideca-1,3,7,11-tetraene, and methyl salicylate. Inhibition of octadecanoid signaling by aristolochic acid and phenidone as well as mass spectrometric analysis of endogenous jasmonate demonstrate that ALA induces the biosynthesis of volatile compounds principally via the octadecanoid-signaling pathway (20-fold increase of jasmonic acid). ALA also up-regulates salicylate biosynthesis, and the time course of the production of endogenous salicylate correlates well with the appearance of the methyl ester in the gas phase. The massive up-regulation of the SA-pathway (90-fold) interferes with steps in the biosynthetic pathway downstream of 12-oxophytodienoic acid and thereby reduces the pattern of emitted volatiles to compounds previously shown to be induced by early octadecanoids. ALA also induces tendril coiling in various species like Pisum, Lathyrus, and Bryonia, but the response appears to be independent from octadecanoid biosynthesis, because inhibitors of lipoxygenase and phospholipase A(2) do not prevent the coiling reaction

Interaction between polygalacturonase-inhibiting protein and jasmonic acid during defense activation in tomato against Botrytis cinerea

Copyright SpringerOligogalacturonic acids (OGAs) generated from in vitro interaction between fungal polygalacturonase (PG) and bean PG-inhibiting protein (PGIP) were shown to activate phytoalexin biosynthesis in soybean. Based on this observation, it was hypothesized that PGIP-dependent generation of OGAs activates plant defence responses in vivo. We tested the hypothesis that PGIP activates jasmonic acid-dependent responses to pathogens. For this purpose, a population of tomato plants segregating for a mutation in the jasmonate receptor CORONATINE INSENSITIVE1 (coi1) and for overexpression of pear PGIP (pPGIP) was challenged with Botrytis cinerea. The coi1 mutant was hypersensitive to B. cinerea, but overexpression of pPGIP in the coi1 mutant background reduced pathogen susceptibility, suggesting that these two genes independently alter defence responses. In addition, pPGIP overexpression suppressed pathogen induction of salicylic acid in the coi1 mutant and activated expression of acidicß-1,3-glucanase independently of the coi1 mutation. However, expression of proteinase inhibitor II (PIN II) in pPGIP overexpressing tomato plants was dependent on COI1. Effects of pPGIP overexpression on defence are therefore complex and only in the case of PIN II pPGIP acts through COI1Peer reviewe