A bacterial receptor PcrK senses the plant hormone cytokinin to promote adaptation to oxidative stress
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ABSTRACT:
PROVIDER: PRJNA415352 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6202170.fastq.gz | Fastqsanger.gz | |||
| SRR6202168.fastq.gz | Fastqsanger.gz | |||
| SRR6202169.fastq.gz | Fastqsanger.gz |
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Project description:By analyzing the transcriptome of WT/ΔpcrR/ΔpcrK strains in the presence of 2iP and comparing gene expression level between them, we report genes with different expression levels between WT and ΔpcrR/ΔpcrK strains in the presence of plant cytokinin 2iP.
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Project description:Oxidative and Cytokinin treatment of Arabidopsis wildtype, crf6 mutant, and CRF6 overexpressing seedlings Arabidopsis seedlings were treated with oxidative stress or cytokinin to determine transcripts altered in each genotype background
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Project description:While the biosynthesis, degradation, and signaling pathways for the essential plant hormone cytokinin have been extensively studied, the direct transcriptional targets of B-type ARRs, the key TFs essential for cytokinin action have not been defined. We epitope tagged four B-ARRs (1, 10, 12, and 14) using recombineering techniques and profiled TF binding sites using chromatin immunoprecipitation sequencing (ChIP-seq). The resulting cytokinin transcriptional response network allowed construction of the first cytokinin TF network, identification of numerous direct downstream targets along with the B-ARR-6BA motif and elucidation of one mechanism of activation of WUSCHEL, which requires a high concentration of cytokinin in shoot apical meristem for TF binding.
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Project description:The transition of skotomorphogenesis to photomorphogenesis is induced by the perception of light and is characterized by the inhibition of hypocotyl elongation and opening of cotyledons. Although it is known that the plant hormone cytokinin, when applied in high concentrations, inhibits hypocotyl elongation in the dark-grown Arabidopsis plants, it is unclear to what extent this response is the result of cytokinin alone or cytokinin-induced ethylene production. We show that treatment of etiolated seedlings in presence of ethylene inhibitors (eg. AgNO3) or treatment of the ethylene-resistant mutant ein2, resulted in a significant inhibition of hypocotyl elongation. This indicates that cytokinin induced de-etiolation is largely independent of ethylene and suggests a close connection between the cytokinin two component system and the light singalling networks. We show that this cytokinin signal is mainly mediated through the cytokinin receptor ARIBIDOPSIS HISTIDIN KINASE 3 (AHK3) and the ARABIDOPSIS RESPONSE REGULATORS 1 (ARR1) in combination with ARR12. Interestingly, mutation of COP1, DET1 and CIN4/COP10 renders plants insensitive to cytokinin and these factors are indispensable for the transcriptional response during cytokinin induced de-etiolation which indicates that a functional light signaling pathway is essential for this cytokinin response. In addition, the cytokinin effect on hypocotyl elongation is highly dependent on the ambient light conditions where higher light intensities causes a switch in the response to CK from an inhibitor to a promoter of hypocotyl elongation.
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Project description:Adaptation of pathogenic Leptospira to oxidative stress
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Project description:Cytokinin is a phytohormone involved in the regulation of diverse developmental and physiological processes in plants. Its potential for biotechnology and development of high-yield and more resilient plants has been recognized, but the molecular mechanisms behind its action are far from understood. In this report, the roots of barley seedling were explored as a new tool to reveal as yet unknown cytokinin-responsive proteins. Significant differences were reproducibly observed for 176 proteins, and at least some of the revealed cytokinin-responsive pathways were confirmed in metabolome analysis, including alterations in phenylpropanoid pathway, amino acid biosynthesis or ROS metabolism. Bioinformatics analysis indicated a significant overlap between cytokinin response and response to abiotic stress. This was confirmed by comparing proteome and metabolome profiles in response to drought, salinity or a period of temperature stress. The results illustrate complex abiotic stress response in the early development of model crop plant and confirm an extensive crosstalk between plant hormone cytokinin and response to temperature stimuli, water availability or salinity.
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Project description:adt05-01_hormon_cells - cyt_aux_balance - Effect of the Auxin/Cytokinin ratio on the transcriptome - Different hormone concentrations were used to grow the cells Keywords: dose response
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Project description:Hormone-dependent protection against oxidative stress in uterine leiomyoma
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Project description:The plant hormone cytokinin regulates diverse aspects of plant growth and development, likely through context-dependent transcriptional regulation that relies on a dynamic interplay between regulatory proteins and chromatin. We employed the Assay for Transposase Accessible Chromatin (ATAC-Seq) to profile changes in the chromatin landscape of Arabidopsis roots and shoots in response to cytokinin. Our results reveal differentially accessible chromatin regions indicative of dynamic regulation in response to cytokinin. These changes in chromatin occur preferentially upstream of genes whose expression changes in response to cytokinin and largely overlap with binding sites for the type-B ARRs, transcription factors that mediate the primary response to cytokinin. Further, the type-B ARRs were found to be necessary for the changes in chromatin state in response to cytokinin. Lastly, we find context-dependent responses by comparing root and shoot profiles. These datasets provide new insights into the transcriptional regulatory mechanisms involved in the cytokinin response and how cytokinin mediates its pleiotropic effects.
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Project description:Context. Uterine leiomyomas exist in a chronically pro-oxidant environment characterized by reduced antioxidant capacity, yet they persist and grow, suggesting the activation of adaptive stress-tolerance mechanisms. Although estrogen and progesterone are central drivers of leiomyoma growth, their role in regulating mitochondrial function under oxidative stress remains incompletely understood. Objective. To investigate how estrogen and progesterone signaling modulate oxidative stress–induced transcriptional programs and mitochondrial metabolic function in uterine leiomyoma cells. Design. Primary patient-derived leiomyoma spheroids were exposed to paraquat-induced oxidative stress in the presence of estradiol, progestins, or hormone receptor antagonists. Transcriptomic responses were assessed by RNA sequencing followed by differential expression and gene set enrichment analyses. Functional mitochondrial metabolism was evaluated using Seahorse extracellular flux assays, and cellular outcomes including senescence and cell death were quantified. Patients. Uterine leiomyoma tissues were obtained from patients undergoing hysterectomy, and primary patient-derived leiomyoma cells were used to generate three-dimensional spheroid cultures. Results. Estradiol and progesterone modulated oxidative stress–responsive transcriptional programs associated with senescence, apoptosis, and mitochondrial regulation. Hormone receptor antagonism induced the most pronounced transcriptomic disruption and was associated with increased senescence and cell death. Consistent with these findings, Seahorse analyses demonstrated that hormonal signaling preserved mitochondrial maximal respiration and spare respiratory capacity under oxidative stress, whereas hormone blockade impaired mitochondrial reserve capacity without compensatory glycolytic upregulation. Progesterone receptor isoform–specific effects further supported a role for differential PR signaling in regulating mitochondrial adaptability. Conclusions. Estrogen and progesterone promote mitochondrial adaptability in leiomyoma cells, enabling survival under sustained oxidative stress. These findings identify mitochondria as a key mediator of hormone-dependent stress resilience and highlight mitochondrial metabolism as a potential therapeutic vulnerability in leiomyomas.
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