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Allantoin, a stress-related purine metabolite, can activate jasmonate signaling in a MYC2-regulated and abscisic acid-dependent manner.

ABSTRACT: Allantoin is a metabolic intermediate of purine catabolism that often accumulates in stressed plants. Recently, we used Arabidopsis knockout mutants (aln) of ALLANTOINASE to show that this purine metabolite activates abscisic acid (ABA) production, thereby stimulating stress-related gene expression and enhancing seedling tolerance to abiotic stress. A detailed re-examination of the microarray data of an aln mutant (aln-1) confirmed the increased expression of ABA-related genes and also revealed altered expression of genes involved in jasmonic acid (JA) responses, probably under the control of MYC2, a master switch in the JA signaling pathway. Consistent with the transcriptome profiles, the aln-1 mutant displayed increased JA levels and enhanced responses to mechanical wounding and exogenous JA. Moreover, aln mutants demonstrated modestly increased susceptibility to Pseudomonas syringae and Pectobacterium carotovorum, probably reflecting the antagonistic action of MYC2 on the defense against these bacterial phytopathogens. Exogenously administered allantoin elicited the expression of JA-responsive genes, including MYC2, in wild-type plants, supporting the idea that allantoin might be responsible for the observed JA-related phenotypes of aln mutants. However, mutants deficient in bioactive JA (jar1-1), insensitive to JA (myc2-3), or deficient in ABA (aba2-1 and bglu18) suppressed the effect of exogenous allantoin. The suppression was further confirmed in aln-1 jar1-1 and aln-1 bglu18 double mutants. These results indicate that allantoin can activate the MYC2-regulated JA signaling pathway through ABA production. Overall, this study suggests a possible connection of purine catabolism with stress hormone homeostasis and signaling, and highlights the potential importance of allantoin in these interactions.

SUBMITTER: Takagi H

PROVIDER: S-EPMC4809300 | biostudies-literature | 2016 Apr

REPOSITORIES: biostudies-literature

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Allantoin, a stress-related purine metabolite, can activate jasmonate signaling in a MYC2-regulated and abscisic acid-dependent manner.

Takagi Hiroshi H Ishiga Yasuhiro Y Watanabe Shunsuke S Konishi Tomokazu T Egusa Mayumi M Akiyoshi Nobuhiro N Matsuura Takakazu T Mori Izumi C IC Hirayama Takashi T Kaminaka Hironori H Shimada Hiroshi H Sakamoto Atsushi A

Journal of experimental botany 20160301 8

Allantoin is a metabolic intermediate of purine catabolism that often accumulates in stressed plants. Recently, we used Arabidopsis knockout mutants (aln) of ALLANTOINASE to show that this purine metabolite activates abscisic acid (ABA) production, thereby stimulating stress-related gene expression and enhancing seedling tolerance to abiotic stress. A detailed re-examination of the microarray data of an aln mutant (aln-1) confirmed the increased expression of ABA-related genes and also revealed ...[more]

PMID: 26931169

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Project description:Allantoin is a metabolic intermediate of purine catabolism that often accumulates in stressed plants. Recently, using Arabidopsis knockout mutants (aln) of ALLANTOINASE, we showed that this purine metabolite activates ABA production, thereby stimulating stress-related gene expression and enhancing seedling tolerance to abiotic stress. A detailed re-examination of the microarray data of an aln mutant (aln-1) not only confirmed increased expression of ABA-inducible genes, but also revealed altered expression of genes involved in jasmonic acid (JA) responses, likely under the control of MYC2, a master switch in the JA signaling pathway. Consistent with the transcriptome profiles, the aln-1 mutant displayed increased JA levels and enhanced responses to mechanical wounding and exogenous JA. Moreover, aln mutants demonstrated modestly increased susceptibility to hemibiotrophic and necrotrophic pathogens, probably reflecting the antagonistic action of MYC2 on the defense against these bacteria. Exogenously administered allantoin elicited the expression of JA-responsive genes including MYC2 in wild-type plants, supporting that allantoin might be responsible for the observed JA-related aln phenotypes. However, the effect of exogenous allantoin was suppressed by mutations deficient in bioactive JA (jar1-1), insensitive to JA (myc2-3) and deficient in ABA (aba2-1 and bglu18). The suppressive effect of jar1-1 and bglu18 mutations was further confirmed in the aln-1 background (jar1-1/aln-1 and bglu18/aln-1). These results indicate that allantoin can activate the MYC2-regulated JA signaling pathway through ABA production. Overall, this study provides evidence for the possible connection of purine catabolism with stress hormone homeostasis and signaling, and highlights the importance of allantoin in these interactions. Evidence has been presented only recently for the involvement of purine catabolism in stress protection of plants and the mechanism behind this remains obscure. Here we show that in Arabidopsis, the intermediary metabolite allantoin can activate the MYC2-regulated jasmonate signaling pathway via the mechanism involving ABA, providing the link between the metabolism and two interactive signaling pathways of stress hormones that play critical roles in plant adaptation to environmental adversity.

Project description:BackgroundMYC2, a basic helix-loop-helix (bHLH) domain-containing transcription factor, participates in the jasmonate (JA) signaling pathway and is involved in the modulation of diverse JA functions. However, a comprehensive list of MYC2-dependent JA-responsive proteins has yet to be defined.ResultsIn this paper, we report the comparative proteomics of wild-type (WT) plants and jin1-9, a MYC2 mutant plant, in response to methyl jasmonate (MeJA) treatment. Proteins from mock/MeJA-treated jin1-9 and WT samples were extracted and separated by two-dimensional gel electrophoresis. Twenty-seven JA-mediated proteins demonstrated differential expression modulated by MYC2. We observed that MYC2 negatively regulates the accumulation of JA-dependent indolic glucosinolate-related proteins and exhibits opposite effects on the biosynthetic enzymes involved aliphatic glucosinolate pathways. In addition, proteins involved in the tricarboxylic acid cycle and a majority of the MeJA-inducible proteins that are involved in multiple protective systems against oxidative stress were reduced in jin1-9/myc2 sample compared to the WT sample. These results support a positive role for MYC2 in regulating JA-mediated carbohydrate metabolism and oxidative stress tolerance.ConclusionsWe have identified MYC2-dependent jasmonate-regulated proteins in Arabidopsis thaliana by performing two-dimensional gel electrophoresis and MALDI-TOF/TOF MS analysis. The observed pattern of protein expression suggests that MYC2 has opposite effects on the biosynthetic enzymes of indolic and aliphatic glucosinolate pathways and positively regulates JA-mediated carbohydrate metabolism and oxidative stress tolerance-related proteins. Furthermore, it is very interesting to note that MYC2 plays opposite roles in the modulation of a subset of JA-regulated photosynthetic proteins during short-term and long-term JA signaling. This study will enhance our understanding of the function of MYC2 in JA signaling in Arabidopsis thaliana.

Dataset Information

Allantoin, a stress-related purine metabolite, can activate jasmonate signaling in a MYC2-regulated and abscisic acid-dependent manner.

Publications

Allantoin, a stress-related purine metabolite, can activate jasmonate signaling in a MYC2-regulated and abscisic acid-dependent manner.

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