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:Regulation of stomatal movement is one of the effective strategies for developing resistant crops to air pollutant because stomata allows absorption of various air pollutants, such as ozone and sulfur dioxide. Transcription factor (TF) is a fascinating target of genetic manipulation for this end because TF regulates many genes simultaneously and methods of genetic manipulation are universally established. Here, we have screened transgenic Arabidopsis lines expressing chimeric repressor of TFs in high-concentration of ozone and found that the chimeric repressors of GOLDEN-LIKE1 (GLK1) and GLK2 (GLK1-SRDX and GLK2-SRDX) conferred strong tolerance to ozone. These 35S:GLK1/2-SRDX plants also showed sulfur dioxide tolerance. Their leaves showed lower rate of transpiration than wild type and a remarkable closed-stomata phenotype. The expression of the genes encoding K+ and water channels, including KAT1 and AKT1, which are involved in stomatal opening, was downregulated in 35S:GLK1-SRDX plants. Consistently, expression of GLK1-SRDX driven by the GC1 promoter, which has an activity only in guard cell, also induced closed-stomata and an ozone tolerant phenotype. On the contrary, 35S:GLK1/2 plants showed hypersensitivity to ozone and an opened-stomata phenotype. These data suggested that GLK1 and GLK2 have an ability to induce transcriptional change in guard cell and regulate stomatal movement. Our findings provide an effective tool to confer resistance to air pollutant by regulating stomatal aperture and improve crop productivity in future.
Project description:To understand the downstream genes of TCP13, we performed analysis of gene expression using vector control plants and the TCP13 fused repression domain plants (TCP13pro::TCP13SRDX) . TheTCP13pro::TCP13SRDX plants is transgenic plants expressing chimeric repressor (SRDX) fused to TCP13 cDNA using the TCP13 promoter. TCP13 is a drought-inducible gene and play an essential role in leaf morphology. Arabidopsis plants were grown on the Murashige and Skoog (MS) medium (Murashige and Skoog, 1962), supplemented with 3% sucrose and 0.8 % agar (under a 16-h-day (60 ± 10 μmol photons m−2 s−1 light intensity) and 8-h-night regime for 2 weeks.
Project description:Proper cell wall regulation is essential for growth and development in plants. Here we report that the constitutive expression of MYB87 chimera repressor causes the suppressed longitudinal organ elongation in almost all organs. Aberrant transversal growth is also observed in multiple organs which coincide with transversally expanded or swollen cells. Microarray analysis revealed the transcript levels of various primary cell wall related enes are up- or down-regulated, and those of secondary wall related genes are down- regulated in the chimera repressor plants. These findings ontribute to the further understanding of complex cell wall regulations and their roles in plant growth and development. Transcriptomes of 35S:MYB87-SRDX and wild-type Arabidopsis seedling were compared.
Project description:Purpose: To understand the molecular mechanism between PNET2 and NTLs, we generated 35S:NTL-SRDX in pnet2_ab mutants to suppress NTL gene expression and performed the whole genome transcriptome analysis on 4-week-old plants of WT, pnet2_ab, 35S:NTL6-SRDX pnet2_ab, 35S:NTL9-SRDX pnet2_ab, and 35S:NTL12-SRDX pnet2_ab. Conclusions: PNET2 regulates diverse responses by associating with a family of membrane-bound transcriptional factors.
Project description:Plants form callus and regenerate new organs when incubated on phytohormone-containing media. While accumulating evidence suggests that these regenerative processes are governed by transcriptional networks orchestrating stress responses and developmental transitions, it remains unknown if post-translational regulatory mechanisms are involved in this process. Here, we find that SIZ1, which encodes an E3 ligase catalyzing attachment of the SMALL UBIQUITIN-LIKE MODIFIER (SUMO) to proteins, regulates wound-induced signal transduction and organ regeneration. We show that loss-of-function mutants for SIZ1 exhibit over-production of shoot meristems under in vitro tissue culture conditions, while this defect is rescued in a complementation line expressing pSIZ1::SIZ1. RNA-sequencing analysis revealed that siz1-2 mutant exhibits enhanced transcriptional responses to wound stress, resulting in the hyper-induction of over 500 genes immediately after wounding. Among them, we show that elevated level of WOUND INDUCED DEDIFFERENTIATION 1 (WIND1) and WIND2 contribute to enhanced shoot regeneration observed in siz1 mutants, as the dominant-negative WIND1-SRDX partly rescues this phenotype in siz1-3. Although compromised SIZ1 function does not modify transcription of genes implicated in auxin-induced callus formation and/or pluripotency acquisition, it does lead to enhanced induction of cytokinin-induced shoot meristem regulators like WUSCHEL (WUS), promoting the formation of WUS-expressing foci in explants. This study thus suggests that SIZ1 negatively regulates shoot regeneration in part by repressing wound-induced cellular reprogramming.