Reversible protein phosphorylation regulates jasmonic acid-dependent and -independent wound signal transduction pathways in Arabidopsis thaliana.
Plants responses to mechanical injury are complex and include the induced expression of defence-related genes. The phytohormone JA has been reported to mediate some of these responses. To elucidate further the signal transduction processes involved, the action of specific agonists and antagonists of known signalling effectors on the response of Arabidopsis thaliana plantlets to JA and wounding was investigated. The identification and characterization of a reversible protein phosphorylation step in a transduction pathway leading to JA-induced gene transcription is reported. This phosphorylation event involved the opposing activities of a staurosporine-sensitive protein kinase, negatively regulating the pathway, and a protein phosphatase, most probably of type 2 A, which activated JA-responsive gene expression. JA activation via this pathway was blocked in the A. thaliana JA-insensitive mutants jin1, jin4 and coi1, and by exogenous application of cycloheximide or auxins. Wound-induced activation of JA-responsive genes was also regulated by this protein phosphorylation step. An alternative wound signalling pathway, independent of JA, was also identified, leading to the transcriptional activation of a different set of genes. This JA-independent pathway was also regulated by a protein phosphorylation switch, in which the protein kinase positively regulated the pathway while the protein phosphatase negatively regulated it. Moreover, a labile protein apparently repressed the expression of these genes. One of the genes analysed, JR3, had a complex pattern of expression, possibly because it was regulated via both of the wound signalling pathways identified. According to the function of an homologous gene, JR3 may be involved in feedback inhibition of the JA response.
Centro Nacional de Biotecnología CSIC, Madrid, Spain.
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Rojo
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Titarenko
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León
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Berger
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Vancanneyt
J J
JJ
Sánchez-Serrano
D017360:Arabidopsis / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism*; D003513:Cycloheximide / Q000494:pharmacology; D003517:Cyclopentanes / Q000494:pharmacology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005246:Feedback; D018506:Gene Expression Regulation, Plant / Q000187:drug effects; D017343:Genes, Plant; D007210:Indoleacetic Acids / Q000494:pharmacology; D008954:Models, Biological; D019319:Okadaic Acid / Q000494:pharmacology; D054883:Oxylipins; D010749:Phosphoprotein Phosphatases / Q000037:antagonists & inhibitors / Q000378:metabolism; D010766:Phosphorylation; D010937:Plant Growth Regulators / Q000494:pharmacology*; D010940:Plant Proteins / Q000378:metabolism*; D047428:Protein Kinase Inhibitors; D011494:Protein Kinases / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D019311:Staurosporine / Q000494:pharmacology; D015533:Transcriptional Activation / Q000187:drug effects
D003517:Cyclopentanes; D004791:Enzyme Inhibitors; D007210:Indoleacetic Acids; D054883:Oxylipins; D010937:Plant Growth Regulators; D010940:Plant Proteins; D047428:Protein Kinase Inhibitors; D019319:Okadaic Acid; C011006:jasmonic acid; D003513:Cycloheximide; D011494:Protein Kinases; D010749:Phosphoprotein Phosphatases; D019311:Staurosporine