Disease relevance of Coronatine

• Activation of a COI1-dependent pathway in Arabidopsis by Pseudomonas syringae type III effectors and coronatine [1].
• We then used Pst DC3000 virulence mutants to characterize Arabidopsis transcriptional responses to the action of hrp-regulated virulence factors (e.g. TTSS and COR) during bacterial infection [2].
• In this study, the effect of coronatine on the development of the chlorotic lesion on the Phaseolus vulgaris L. leaves, indicates that coronatine induced chlorosis on treated leaves as well as or untreated leaves on the same plant [3].

High impact information on Coronatine

• The coronatine and syringomycin gene clusters have been intensively characterized and show potential for constructing modified polyketides and peptides [4].
• COS1: an Arabidopsis coronatine insensitive1 suppressor essential for regulation of jasmonate-mediated plant defense and senescence [5].
• This was correlated with increased larval performance on the coronatine insensitive1 glabrous1 (coi1-1 gl1) mutant [6].
• JIN1 encodes AtMYC2, a nuclear-localized basic helix-loop-helix-leucine zipper transcription factor, whose expression is rapidly upregulated by JA, in a CORONATINE INSENSITIVE1-dependent manner [7].
• In addition, the purified phytotoxin coronatine, a known virulence factor of P. syringae, suppresses the flagellin-induced NHO1 transcription [8].

Chemical compound and disease context of Coronatine

• The phytotoxic principle, coronatine, which is present in several pathovars of the plant pathogen, Pseudomonas syringae was shown to be highly active in completely different, jasmonate-selective bioassays [9].
• Coronafacic acid (CFA) is the polyketide component of coronatine (COR), a phytotoxin produced by the plant-pathogenic bacterium Pseudomonas syringae [10].
• Coronamic acid (CMA), an ethylcyclopropyl amino acid derived from isoleucine, functions as an intermediate in the biosynthesis of coronatine, a chlorosis-inducing phytotoxin produced by Pseudomonas syringae pv. glycinea PG4180 [11].
• The Pseudomonas phytotoxin coronatine induces ethylene biosynthesis and diseaselike symptoms on many plant species, but the reduced symptomology of ein2 mutants could not be attributed to insensitivity to coronatine [12].

Biological context of Coronatine

• Coronatine-triggered and spontaneous lesion spreading in acd2 plants also requires protein translation, indicating that cell death occurs by an active process [13].
• The amino acid sequence shared 37% identity with a function-unknown gene whose mRNA is inducible by coronatine and methyl jasmonate (MeJA) in Arabidopsis thaliana (AtCLH1) [14].
• However, little is known about the interplay between the host gene expression changes associated with basal defenses and the virulence activities of the TTSS and COR during infection [2].
• 2. This plasmid was introduced into P. syringae pv. syringae PS61, which does not produce coronatine [15].
• Biological activity critically depended upon the structure of coronatine, and slight modifications, such as methylation of the carboxyl moiety or reduction of the carbonyl group, rendered the molecules almost inactive [9].

Associations of Coronatine with other chemical compounds

• Differential expression of a novel gene in response to coronatine, methyl jasmonate, and wounding in the Coi1 mutant of Arabidopsis [16].
• Characterization and transcriptional analysis of the gene cluster for coronafacic acid, the polyketide component of the phytotoxin coronatine [17].
• In contrast to wild-type ES4326, ES4326 rpoN::Km(r) was nonmotile and could not utilize nitrate, urea, C(4)-dicarboxylic acids, several amino acids, or concentrations of ammonia below 2 mM as nitrogen sources. rpoN was essential for production of the phytotoxin coronatine and for expression of the structural genes encoding coronamic acid [18].
• On the other hand, coronatine, a phytotoxin mimicking octadecanoids and leading to symptoms of senescence, caused a moderate increase in alpha-tocopherol as well as some enhancement of gamma-tocopherol [19].

Gene context of Coronatine

• These results suggest that P. syringae type III effectors and coronatine act by augmenting a COI1-dependent pathway to promote parasitism [1].
• Soluble recombinant CORI1 was purified and shown to possess chlorophyllase (Chlase) activity in vitro [20].
• Given that tvrR mutant strains are not defective for type III secretion or COR production, tvrR appears to be a novel virulence factor required for a previously unexplored process that is necessary for pathogenesis [21].
• Regulation of plant arginase by wounding, jasmonate, and the phytotoxin coronatine [22].
• Analyses of P. syringae pv. tomato DC3000 mutants indicated that both type III secretion system and the phytotoxin coronatine are required for RAP2.6 induction [1].

Analytical, diagnostic and therapeutic context of Coronatine

• Sequence analysis of 79 fusions revealed several known and potential virulence genes, including hrp/hrc, avr and coronatine biosynthetic genes [23].
• The primer set amplified diagnostic 0.65-kb PCR products from genomic DNAs of five different coronatine-producing pathovars of P. syringae [24].
• At nanomolar to micromolar concentrations, coronatine induced the accumulation of defense-related secondary metabolites in several plant cell cultures, induced transcript accumulation of the elicitor-responsive gene encoding the berberine bridge enzyme of Eschscholtzia californica, as well as the coiling response of Bryonia dioica tendrils [9].
• A bioassay for coronatine suggested that PS61(pPT23A) transconjugants were able to make this phytotoxin [15].
• The effect of each mutation on coronatine synthesis was determined by analyzing the organic acids produced by the mutants by reverse-phase high-performance liquid chromatography [25].

References