Arabidopsis thaliana
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ABSTRACT:
PROVIDER: PRJNA298207 | ENA |
REPOSITORIES: ENA
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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.
2016-03-01 | E-GEOD-73841 | biostudies-arrayexpress
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.
2016-03-01 | GSE73841 | GEO
Project description:The Jasmonate pathway regulators MYC2, MYC3 and MYC4 are central nodes in plant signaling networks integrating environmental and developmental signals to fine-tune jasmonate defenses and plant growth. Hence, their activity needs to be tightly regulated in order to optimize plant fitness. Among the increasing number of mechanisms regulating MYCs, protein stability is arising as a major player. However, how the levels of MYCs proteins are modulated is still poorly understood. Here, we report that MYC2, MYC3 and MYC4 are targets of BPM proteins, which act as substrate adaptors of CUL3-based E3 ubiquitin ligases. Reduction-of-function of CUL3(BPM) in amiR-bpm lines, bpm235 triple mutants and cul3ab double mutants enhance MYC2 and MYC3 stability and accumulation, and potentiates plant responses to JA such a root-growth inhibition, and MYC-regulated gene expression. BPM3 protein is stabilized by JA, suggesting a new negative feedback regulatory mechanism to control MYCs activity. Our results uncover a new layer for JA-pathway regulation by CUL3(BPM)-mediated degradation of MYC TFs.
2021-03-19 | PXD013906 | Pride
Project description:The Jasmonate pathway regulators MYC2, MYC3 and MYC4 are central nodes in plant signaling networks integrating environmental and developmental signals to fine-tune jasmonate defenses and plant growth. Hence, their activity needs to be tightly regulated in order to optimize plant fitness. Among the increasing number of mechanisms regulating MYCs activity, protein stability is arising as a major player. However, how the levels of MYCs proteins are modulated is still poorly understood. Here, we report that MYC2, MYC3 and MYC4 are targets of BPM proteins, which act as substrate adaptors of CUL3-based E3 ubiquitin ligases. Reduction-of-function of CUL3BPM in amiR-bpm lines, bpm235 triple mutants and cul3ab double mutants enhances MYC2 and MYC3 stability and accumulation, and potentiates plant responses to JA such as root-growth inhibition, and MYC-regulated gene expression. BPM3 protein is stabilized by JA, suggesting a new negative feed-back regulatory mechanism to control MYCs activity. Our results uncover a new layer for JA-pathway regulation by CUL3BPM–mediated degradation of MYC TFs.
2020-02-09 | GSE131037 | GEO
Project description:The Jasmonate pathway regulators MYC2, MYC3 and MYC4 are central nodes in plant signaling networks integrating environmental and developmental signals to fine-tune jasmonate defenses and plant growth. Hence, their activity needs to be tightly regulated in order to optimize plant fitness. Among the increasing number of mechanisms regulating MYCs activity, protein stability is arising as a major player. However, how the levels of MYCs proteins are modulated is still poorly understood. Here, we report that MYC2, MYC3 and MYC4 are targets of BPM proteins, which act as substrate adaptors of CUL3-based E3 ubiquitin ligases. Reduction-of-function of CUL3BPM in amiR-bpm lines, bpm235 triple mutants and cul3ab double mutants enhances MYC2 and MYC3 stability and accumulation, and potentiates plant responses to JA such as root-growth inhibition, and MYC-regulated gene expression. BPM3 protein is stabilized by JA, suggesting a new negative feed-back regulatory mechanism to control MYCs activity. Our results uncover a new layer for JA-pathway regulation by CUL3BPM–mediated degradation of MYC TFs.
2020-02-09 | GSE131024 | GEO
Project description:Plants trigger leaf senescence to relocate energy and nutrients from aging leaves to developing tissues or storage organs to optimize the growth and reproduction under limited nutrients and energy conditions. Jasmonate signaling is one of the major endogenous hormone signals to induced leaf senescence in Arabidopsis. However, whether circadian clock will gate Jasmonate signaling to induce leaf senescence and the underlying precise mechanism is unclear. Here we find that the Evening Complex (EC) of core oscillator closely regulates leaf senescence. To identify the underlying mechanism of EC regulating leaf senescence, we conducted RNA-sequencing. Transcriptomic data reveals Evening complex extensively involves into JA signal transduction and responses. Moreover, the mutants of ELF3, ELF4 and LUX universly display the accelerated JA-induced leaf senescence phenotype, while their overexpression lines act reversely. In accordance with the transcript levels of JA immediate early induced JA-responsive gene MYC2 are up-regulated in lux mutants. Futhermore we demonstrated LUX can bind to to the promoter of MYC2 in vivo to represses its transcription. In addition, the accelerated JA-induced leaf senescence in mutants of evening complex can be overturned by myc2, myc3 and myc4 mutants redundantly. Collectively, our findings demonstrated the underlying molecular basis for circadian clock gating jasmonate signaling to induce leaf senescence through the module of evening complex to directly repressing MYC2 transcription. This novel established molecular module also refines complicated nodes between circadian clock and jasmonate signal in Arabidopsis.
2018-02-06 | GSE99290 | GEO
Project description:Purine catabolism is regarded as a housekeeping function that remobilizes nitrogen for plant growth and development. However, emerging evidence suggests that certain purine metabolites might contribute to stress protection of plants. Here, we show that in Arabidopsis, the intermediary metabolite allantoin plays a role in abiotic stress tolerance via activation of abscisic acid (ABA) metabolism. The aln loss-of-function of ALN, encoding allantoinase, results in increased allantoin accumulation, genome-wide up-regulation of stress-related genes, and enhanced tolerance to drought-shock and osmotic stress in aln mutant seedlings. This phenotype is not caused by a general response to purine catabolism inhibition, but rather results from a specific effect of allantoin. Allantoin activates ABA production both through increased transcription of NCED3, encoding a key enzyme in ABA biosynthesis, and through post-translational activation via high-molecular-weight complex formation of BG1, a ß-glucosidase hydrolyzing glucose-conjugated ABA. Exogenous application of allantoin to wild-type plants also activates the two ABA-producing pathways that lead to ABA accumulation and stress-responsive gene expression, but this effect is abrogated in ABA-deficient and BG1-knockout mutants. We propose that purine catabolism functions not only in nitrogen metabolism, but also in stress tolerance by influencing ABA production, which is mediated by the possible regulatory action of allantoin. Compared analysis of the transcriptomes of 2-week-old Arabidopsis seedlings from an allantoin-accumulating mutant genotype versus wild type background Col-0 (2 independent biological replicates per genotype). The allantoin-accumulating mutant in Col-0 background was the aln-1 mutant allele in allantoinase (ALN) (abbreviated as aln).
2014-01-16 | E-GEOD-44922 | biostudies-arrayexpress
Project description:Purine catabolism is regarded as a housekeeping function that remobilizes nitrogen for plant growth and development. However, emerging evidence suggests that certain purine metabolites might contribute to stress protection of plants. Here, we show that in Arabidopsis, the intermediary metabolite allantoin plays a role in abiotic stress tolerance via activation of abscisic acid (ABA) metabolism. The aln loss-of-function of ALN, encoding allantoinase, results in increased allantoin accumulation, genome-wide up-regulation of stress-related genes, and enhanced tolerance to drought-shock and osmotic stress in aln mutant seedlings. This phenotype is not caused by a general response to purine catabolism inhibition, but rather results from a specific effect of allantoin. Allantoin activates ABA production both through increased transcription of NCED3, encoding a key enzyme in ABA biosynthesis, and through post-translational activation via high-molecular-weight complex formation of BG1, a ß-glucosidase hydrolyzing glucose-conjugated ABA. Exogenous application of allantoin to wild-type plants also activates the two ABA-producing pathways that lead to ABA accumulation and stress-responsive gene expression, but this effect is abrogated in ABA-deficient and BG1-knockout mutants. We propose that purine catabolism functions not only in nitrogen metabolism, but also in stress tolerance by influencing ABA production, which is mediated by the possible regulatory action of allantoin.
2014-01-16 | GSE44922 | GEO
Project description:The purine signaling pathway is crucial for cellular function and is a conserved metabolic network from prokaryotes to humans. While extensively studied in microorganisms like yeast and bacteria, the impact of perturbing dietary intermediates from the purine signaling pathway on animal development and growth remains poorly understood. We utilized Caenorhabditis elegans as the metazoan model to investigate the mechanisms underlying this deficiency. Through a high-throughput screening of an E. coli mutant library Keio collection, we identified 34 E. coli mutants that delay C. elegans development. Among these mutants, we found that E. coli purE gene is an essential genetic component that promotes host development in a dose-dependent manner. Further metabolites supplementation suggests that bacterial purE downstream metabolite 5-aminoimidazole-4-carboxamide ribotide (AICAR) can inhibit worm growth. Additionally, we found the FoxO transcription factor DAF-16 is indispensable in worm development delay induced by purE mutation, and observed increased nuclear accumulation of DAF-16 when fed E. coli purE- mutants, suggesting the role of DAF-16 in response to purE mutation. RNA-seq analysis and phenotypic assays revealed that worms fed the E. coli purE mutant exhibited elevated lifespan, thermotolerance, and pathogen resistance. These findings collectively suggest that certain intermediates in the bacterial purine signaling pathway can serve as a cue to modulate development and activate the defense response in the nematode C. elegans through DAF-16.
2024-10-06 | GSE278640 | GEO
Project description:Plants are continuously exposed to environmental triggers, including mechanical stimulation. Our results demonstrate that jasmonic acid (JA)-signalling plays a key role in very early gene expression changes, well before it leads to touch-induced developmental changes. We show that the JA-activated transcription factors MYC2/MYC3/MYC4 co-regulate touch-induced gene expression of 266 genes, many of which peak in induction around 25 minutes and then rapidly decline by 40-60 minutes. ChIP-seq shows that MYC2 dynamically binds hundreds of touch-induced promoters within 25 minutes. Promoter activation assays confirm that MYC2 directly activates these touch-induced promoters. By combining multi-omic data, we have identified a core MYC2/3/4-dependent ‘touch regulon’, containing many previously-unknown MYC2 targets like bHLH19 and ERF109. We show bHLH19 can in turn directly activate the ORA47 promoter, indicating that MYC2/3/4 initiate a hierarchical network of downstream transcription factors. Through hormone profiling we reveal the rapid touch-induced accumulation of JA/JA-isoleucine is directly controlled by MYC2/3/4 in a positive amplification loop regulating JA-biosynthesis genes.
2019-10-29 | PXD014008 | Pride