Disease relevance of JAR1

• JAR1-dependent suppression of the ET pathway was apparent also as increased EIN2-dependent gene expression and ET hypersensitivity of jar1 [1].

High impact information on JAR1

• Genetic analysis indicated that FIN219 interacts closely with another phytochrome A signaling component, FHY1 [2].
• Molecular characterization of FIN219 indicated that it encodes a cytoplasmic localized protein highly similar to the GH3 family of proteins and its expression is rapidly induced by auxin [2].
• In contrast to its loss-of-function mutant phenotype, overexpression of FIN219 results in a far-red-specific hyperphotomorphogenic response [2].
• Jasmonate response locus JAR1 and several related Arabidopsis genes encode enzymes of the firefly luciferase superfamily that show activity on jasmonic, salicylic, and indole-3-acetic acids in an assay for adenylation [3].
• Analysis of fold predictions for this protein family suggested that JAR1 might belong to the acyl adenylate-forming firefly luciferase superfamily [3].

Biological context of JAR1

• This suggests that EIN2 function is epistatic to JAR1, and that the JAR1-dependent JA pathway halts oxidative cell death by directly inhibiting ET signaling [1].
• Our results further indicate that JAR1, as OST1, functions upstream of ROS produced by NAD(P)H oxidases and that the cytoplasmic alkalization precedes ROS production during MJ or ABA signal transduction in guard cells [4].
• The jasmonate (JA)-insensitive mutant jar1 showed normal induction kinetics for both GSTs [5].

Associations of JAR1 with chemical compounds

• JAR1 is 1 of 19 closely related Arabidopsis genes that are similar to the auxin-induced soybean GH3 gene [3].
• RPP7 resistance was also not compromised by mutations in EIN2, JAR1 or COI1 which affect ethylene or jasmonic acid signaling [6].
• An ethyl methanesulfonate mutant (jar1) with decreased sensitivity to MeJA inhibition of root elongation was isolated and characterized [7].
• In contrast, seeds of jar1 plants were more sensitive than wild type to inhibition of germination by abscisic acid [7].
• Gene expression analysis of 1-aminocyclopropane-1-carboxylic acid (ACC)-treated and O(3)-exposed ein2 and jar1 revealed reciprocal antagonism: the EIN2-mediated suppression of the JA pathway [1].

Other interactions of JAR1

• Further phenotypic analyses of this new mutation, named fin219, suggested that it defines a novel phytochrome A signaling component [2].
• Furthermore, the response to far-red light depended on functional FHY1 but not on FIN219 and FHY3 [8].

Analytical, diagnostic and therapeutic context of JAR1

• Thin-layer chromatography and gas chromatography-mass spectrometry (GC-MS) analysis of products produced in vitro by recombinant JAR1 demonstrated that this enzyme forms JA-amido conjugates with several amino acids, including JA-Ile [9].

References