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.
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.
Project description:MYC2 is a central node controlling the crosstalk between JA and other phytohormone signalling pathways and regulating responses to light and circadian clock. We hypothesized that this transcription factor might coordinate prioritization of microbiota-induced growth over defense under suboptimal light conditions
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.
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: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.
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:In symbiotic plant-microbe interactions, the host invests considerable amounts of resources in the microbial partner. If the microbe does not reciprocate with a comparable symbiotic benefit it is regarded as a cheater. The host responds to cheaters with negative feedback mechanisms (sanctions) to prevent fitness deficits resulting from being exploited. We study sanctioning in the symbiosis between Medicago truncatula and the nitrogen-fixing rhizobium Sinorhizobium meliloti. We manipulate the exchange of resources between the partners in three ways, by (i) using mutant rhizobia defective in nitrogenase, (ii) replacing nitrogen in the atmosphere with argon gas; and (iii) supplying rich nitrogen fertilizer to the host. We follow the consequences of simulated cheating by examining the metabolome and proteome of both partners. We find that sanctioning occurs at different levels. In particular, we observe repression of essential symbiotic functions and changes in central metabolism that are likely to be relevant for microbial fitness and that could therefore contribute to sanctioning. In addition, sanctioning triggers a broad panel of defense markers. A thorough understanding of the multi-level phenomenon of sanctioning will be essential for its genetic dissection and for breeding of elite legume crops with efficient symbiosis.
Project description:In symbiotic plant-microbe interactions, the host invests considerable amounts of resources in the microbial partner. If the microbe does not reciprocate with a comparable symbiotic benefit it is regarded as a cheater. The host responds to cheaters with negative feedback mechanisms (sanctions) to prevent fitness deficits resulting from being exploited. We study sanctioning in the symbiosis between Medicago truncatula and the nitrogen-fixing rhizobium Sinorhizobium meliloti. We manipulate the exchange of resources between the partners in three ways, by (i) using mutant rhizobia defective in nitrogenase, (ii) replacing nitrogen in the atmosphere with argon gas; and (iii) supplying rich nitrogen fertilizer to the host. We follow the consequences of simulated cheating by examining the metabolome and proteome of both partners. We find that sanctioning occurs at different levels. In particular, we observe repression of essential symbiotic functions and changes in central metabolism that are likely to be relevant for microbial fitness and that could therefore contribute to sanctioning. In addition, sanctioning triggers a broad panel of defense markers. A thorough understanding of the multi-level phenomenon of sanctioning will be essential for its genetic dissection and for breeding of elite legume crops with efficient symbiosis.
Project description:In symbiotic plant-microbe interactions, the host invests considerable amounts of resources in the microbial partner. If the microbe does not reciprocate with a comparable symbiotic benefit it is regarded as a cheater. The host responds to cheaters with negative feedback mechanisms (sanctions) to prevent fitness deficits resulting from being exploited. We study sanctioning in the symbiosis between Medicago truncatula and the nitrogen-fixing rhizobium Sinorhizobium meliloti. We manipulate the exchange of resources between the partners in three ways, by (i) using mutant rhizobia defective in nitrogenase, (ii) replacing nitrogen in the atmosphere with argon gas; and (iii) supplying rich nitrogen fertilizer to the host. We follow the consequences of simulated cheating by examining the metabolome and proteome of both partners. We find that sanctioning occurs at different levels. In particular, we observe repression of essential symbiotic functions and changes in central metabolism that are likely to be relevant for microbial fitness and that could therefore contribute to sanctioning. In addition, sanctioning triggers a broad panel of defense markers. A thorough understanding of the multi-level phenomenon of sanctioning will be essential for its genetic dissection and for breeding of elite legume crops with efficient symbiosis.