camalexin has been researched along with indoleacetic-acid* in 4 studies
1 review(s) available for camalexin and indoleacetic-acid
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The biosynthesis of shikimate metabolites.
Topics: 3-Deoxy-7-Phosphoheptulonate Synthase; 3-Phosphoshikimate 1-Carboxyvinyltransferase; Alkyl and Aryl Transferases; Animals; Anthranilate Synthase; Bacteria; Betalains; Catalysis; Chorismate Mutase; Coumarins; Flavonoids; Hydro-Lyases; Indoleacetic Acids; Indoles; Intramolecular Transferases; Lignans; Molecular Structure; Penicillium; Phenylalanine; Phenylpropionates; Phosphorus-Oxygen Lyases; Prephenate Dehydratase; Prephenate Dehydrogenase; Pristinamycin; Pyrrolnitrin; Quaternary Ammonium Compounds; Quinones; Shikimic Acid; Staurosporine; Tannins; Thiazoles; Thyroxine; Tryptophan; Tyrosine; Ubiquinone | 2001 |
3 other study(ies) available for camalexin and indoleacetic-acid
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Classic myrosinase-dependent degradation of indole glucosinolate attenuates fumonisin B1-induced programmed cell death in Arabidopsis.
The mycotoxin fumonisin B1 (FB1) causes the accumulation of reactive oxygen species (ROS) which then leads to programmed cell death (PCD) in Arabidopsis. In the process of studying FB1-induced biosynthesis of glucosinolates, we found that indole glucosinolate (IGS) is involved in attenuating FB1-induced PCD. Treatment with FB1 elevates the expression of genes related to the biosynthesis of camalexin and IGS. Mutants deficient in aliphatic glucosinolate (AGS) or camalexin biosynthesis display similar lesions to Col-0 upon FB1 infiltration; however, the cyp79B2 cyp79B3 double mutant, which lacks induction of both IGS and camalexin, displays more severe lesions. Based on the fact that the classic myrosinase β-thioglucoside glucohydrolase (TGG)-deficient double mutant tgg1 tgg2, rather than atypical myrosinase-deficient mutant pen2-2, is more sensitive to FB1 than Col-0, and the elevated expression of TGG1, but not of PEN2, correlates with the decrease in IGS, we conclude that TGG-dependent IGS hydrolysis is involved in FB1-induced PCD. Indole-3-acetonitrile (IAN) and indole-3-carbinol (I3C), the common derivatives of IGS, were used in feeding experiments, and this rescued the severe cell death phenotype, which is associated with reduced accumulation of ROS as well as increased activity of antioxidant enzymes and ROS-scavenging ability. Despite the involvement of indole-3-acetic acid (IAA) in restricting FB1-induced PCD, feeding of IAN and I3C attenuated FB1-induced PCD in the IAA receptor mutant tir1-1 just as in Col-0. Taken together, our results indicate that TGG-catalyzed breakdown products of IGS decrease the accumulation of ROS by their antioxidant behavior, and attenuate FB1 induced PCD in an IAA-independent way. Topics: Arabidopsis; Arabidopsis Proteins; Cell Death; Cytochrome P-450 Enzyme System; Fumonisins; Glucosinolates; Glycoside Hydrolases; Indoleacetic Acids; Indoles; Mutation; Thiazoles | 2015 |
The conjugated auxin indole-3-acetic acid-aspartic acid promotes plant disease development.
Auxin is a pivotal plant hormone that regulates many aspects of plant growth and development. Auxin signaling is also known to promote plant disease caused by plant pathogens. However, the mechanism by which this hormone confers susceptibility to pathogens is not well understood. Here, we present evidence that fungal and bacterial plant pathogens hijack the host auxin metabolism in Arabidopsis thaliana, leading to the accumulation of a conjugated form of the hormone, indole-3-acetic acid (IAA)-Asp, to promote disease development. We also show that IAA-Asp increases pathogen progression in the plant by regulating the transcription of virulence genes. These data highlight a novel mechanism to promote plant susceptibility to pathogens through auxin conjugation. Topics: Arabidopsis; Arabidopsis Proteins; Aspartic Acid; Botrytis; Cyclopentanes; Gene Expression Regulation, Plant; Host-Pathogen Interactions; Indoleacetic Acids; Indoles; Oxylipins; Plant Diseases; Plant Growth Regulators; Pseudomonas syringae; Salicylic Acid; Signal Transduction; Thiazoles; Virulence | 2012 |
Controlled indole-3-acetaldoxime production through ethanol-induced expression of CYP79B2.
Indole-3-acetaldoxime (IAOx) is a key branching point between primary and secondary metabolism. IAOx serves as an intermediate in the biosynthesis of indole glucosinolates (I-GLSs), camalexin and the plant hormone indole-3-acetic acid (IAA). The cytochrome P450s CYP79B2 and CYP79B3 catalyze the conversion of tryptophan to IAOx. CYP83B1 channels IAOx into I-GLS biosynthesis, CYP71A13 channels IAOx into camalexin biosynthesis, whereas the IAOx-metabolizing enzyme in IAA biosynthesis is not known. In this report, we demonstrate controlled production of I-GLSs by introducing an ethanol (EtOH)-inducible CYP79B2 construct into double (cyp79b2 cyp79b3) or triple (cyp79b2 cyp79b3 cyp83b1) mutant lines. We show EtOH-dependent induction of camalexin and identify a number of candidate IAA homeostasis- or defense-related genes by clustered microarray analysis. The transgenic mutant lines are thus promising tools for elucidating the interplay between primary and secondary metabolism. Topics: Arabidopsis; Arabidopsis Proteins; Biosynthetic Pathways; Chromatography, Liquid; Cluster Analysis; Cytochrome P-450 Enzyme System; Ethanol; Gene Expression Profiling; Gene Expression Regulation, Enzymologic; Gene Expression Regulation, Plant; Glucosinolates; Indoleacetic Acids; Indoles; Mass Spectrometry; Molecular Structure; Mutation; Oligonucleotide Array Sequence Analysis; Oximes; Plants, Genetically Modified; Thiazoles | 2009 |