Transcriptional response of A. thaliana Root and Shoot tissue to light stress and presence of microbial communities in myc2-3 and MYC2-Flag lines
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ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE160115 | GEO | 2020/10/27
REPOSITORIES: GEO
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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
Project description:Plants are continuously exposed to environmental triggers, including mechanical stimulation. Our results demonstrate that jasmonic acid (JA)-signalling not only plays a key role in touch-induced developmental changes, but also in the very early gene expression changes. Using multi-omics, we show that the JA-activated transcription factors MYC2/MYC3/MYC4 co-regulate touch-induced gene expression of 266 genes. MYC2/3/4 particularly activate top touch-induced genes, which peak 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. Furthermore, promoter activation assays confirm that MYC2 directly activates touch-induced promoters. By combining these data, we identified a core MYC2/3/4-dependent ‘touch regulon’, containing many previously-unknown MYC2 targets like bHLH19 and ERF109. bHLH19 can in turn directly activate the ORA47 promoter, indicating that MYC2/3/4 initiate a hierarchical network of downstream transcription factors. Finally, hormone profiling shows that 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 | GSE132316 | GEO
Project description:Jasmonate (JA) is a plant hormone that controls trade-offs between plant growth and responses to biotic and abiotic stresses. Although recent studies uncover core mechanism for JA-induced responses in Arabidopsis thaliana, it remains elusive how plants attenuate those responses. We report here that a basic-helix-loop-helix type transcription factor named JA-INDUCIBLE MYC2-LIKE1 (JAM1) acts as a transcriptional repressor and negatively regulates JA signaling. Arabidopsis plants expressing the chimeric repressor for JAM1 exhibited a substantial reduction of JA responses, including JA-induced inhibition of root growth, accumulation of anthocyanin, and male fertility. These plants were also compromised in resistance to attack by Spodoptera exigua. Conversely, jam1-4 loss-of-function mutants showed enhanced JA responsiveness, including increased resistance to the insect attack. Competitive binding of JAM1 and MYC2 to the target sequence of MYC2 suggested negative regulation of JA signaling by JAM1 and suppression of MYC2 function. These results indicate that JAM1 plays a pivotal role in fine-tuning of JA-mediated stress responses and plant growth by negatively regulating JA signaling. Transcriptomes of ProJAM1:JAM1-SRDX, ProMYC2:MYC2-SRDX and wild-type Arabidopsis seedlings with or without jasmonic acid were compared.
2013-07-03 | E-GEOD-42552 | biostudies-arrayexpress
Project description:Jasmonate (JA) is a plant hormone that controls trade-offs between plant growth and responses to biotic and abiotic stresses. Although recent studies uncover core mechanism for JA-induced responses in Arabidopsis thaliana, it remains elusive how plants attenuate those responses. We report here that a basic-helix-loop-helix type transcription factor named JA-INDUCIBLE MYC2-LIKE1 (JAM1) acts as a transcriptional repressor and negatively regulates JA signaling. Arabidopsis plants expressing the chimeric repressor for JAM1 exhibited a substantial reduction of JA responses, including JA-induced inhibition of root growth, accumulation of anthocyanin, and male fertility. These plants were also compromised in resistance to attack by Spodoptera exigua. Conversely, jam1-4 loss-of-function mutants showed enhanced JA responsiveness, including increased resistance to the insect attack. Competitive binding of JAM1 and MYC2 to the target sequence of MYC2 suggested negative regulation of JA signaling by JAM1 and suppression of MYC2 function. These results indicate that JAM1 plays a pivotal role in fine-tuning of JA-mediated stress responses and plant growth by negatively regulating JA signaling.
2013-07-03 | GSE42552 | GEO
Project description:The genome-wide target genes of transcription factors MYC2 and MYC3 were determined in etiolated (dark-grown) seedlings of Arabidopsis thaliana. Chromatin immunoprecipition of MYC2 and MYC3 was performed as described in O’Malley et al (2016; doi: 10.1016/j.cell.2016.04.038), using transgenic A. thaliana expressing MYC2::YpET and MYC3::YpET fusion proteins from their native promoters, generated by recombineering (Gimenez-Ibanez et al. 2017; doi: 10.1111/nph.14354 ). Three-day old etiolated seedlings were treated with methyl JA for 2 h (as described in Schweizer et al., 2013), then harvested for ChIP-Seq.
2019-11-28 | GSE114430 | GEO
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: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: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:Transcriptional response of A. thaliana Root and Shoot tissue to light stress and presence of microbial communities in myc2-3 and MYC2-Flag lines
| PRJNA671872 | ENA
Project description:The hormone jasmonic acid (JA) controls a plethora of crucially important processes in plants through a signaling pathway orchestrated by the transcription factor MYC2 and its closest relatives. Understanding the systems-level actions of transcription factors provides insight into how the genome is reprogrammed in response to environmental stimuli. However, deeper biological insight can be obtained if transcription factor activity is set in the broader regulatory context of the cell and the downstream organismal phenotypes the transcription factors control. Here, we have investigated the MYC2-governed genome regulatory network that controls JA responses in Arabidopsis thaliana etiolated seedlings. We have generated an integrated framework of the response to JA that spans from the activity of master and secondary-regulatory transcription factors, through gene expression outputs and alternative splicing to protein abundance changes, protein phosphorylation and chromatin remodeling. We have integrated time series transcriptome analysis with (phospho)proteomic data using gene regulatory network models. These enable us to predict previously unknown points of crosstalk from JA to other signaling pathways and to identify new components of the JA regulatory mechanism, which we validated through targeted mutant studies. The result is a comprehensive understanding of how a plant hormone remodels cellular function and plant behavior, the general principles of which provide a framework for analysis of cross-regulation between other hormone and stress signaling pathways.
2020-03-13 | GSE133408 | GEO