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The purine metabolite allantoin can activate the jasmonate signaling pathway in a MYC2-regulated and ABA-dependent manner

ABSTRACT: 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.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE73841 | GEO | 2016/03/01

SECONDARY ACCESSION(S): PRJNA298207

REPOSITORIES: GEO

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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. Two replicates of the mutant were compared with controls. This series is a re-analysis of GSE44922.

Project description:Resistance (R) genes are very effective for disease control in plants. Current research shows that R genes predominantly function by inducing a hypersensitive reaction (HR), which results in localized cell death thought to restrict pathogen spread. Some R genes elicit a more atypical response where resistance is not associated with HR or the associated gene expression changes, termed extreme resistance (ER). The molecular regulatory mechanism underlying ER is largely unexplored. One of the few known, naturally occurring, instances of ER is resistance derived from the soybean Rsv3 gene, which confers resistance against the most virulent strains of soybean mosaic virus (SMV). To discern the regulatory mechanism underlying the Rsv3-mediated ER reaction, we generated a gene regulatory network using transcriptomic data from a time course comparison of SMV-G7-infected resistant (L29, Rsv3-genotype) and susceptible (Williams82, rsv3-genotype) soybean cultivars. We identified putative interactions between transcription factors (TFs) regulating gene expression in hormone regulatory pathways, such as abscisic acid (ABA) and jasmonic acid (JA). This is consistent with the demonstrated involvement of these pathways in Rsv3-mediated resistance. We found significant enrichment for the G-box motif (“CACGTG”) among genes implicated in ABA- and JA-related activities. This motif is specifically recognized by MYC2, which is a master regulator of ABA and JA signaling. Our network identified a MYC2 TF encoded by Glyma.07G051500 as a putative transcriptional regulator whose expression was significantly down-regulated in L29. This correlated with the down-regulation of expression of genes involved in ABA and JA processes. Our results suggest an important function for Glyma.07G051500 in ABA and JA derived defense signaling. Additionally, our regulatory network found other putative TFs with differential expression, such as MYBs and ERFs, which may also be involved in regulating ABA and JA signaling for defense. The regulatory network presented here offers new insights into the regulation of the molecular defense mechanism underlying Rsv3-mediated ER against SMV.

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The purine metabolite allantoin can activate the jasmonate signaling pathway in a MYC2-regulated and ABA-dependent manner

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