Oxygen-sensing through ERFVII action and modulation in Arabidopsis thaliana
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA932223 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23357700_1.fastq.gz | Fastqsanger.gz | |||
| SRR23357700_2.fastq.gz | Fastqsanger.gz | |||
| SRR23357701_1.fastq.gz | Fastqsanger.gz | |||
| SRR23357701_2.fastq.gz | Fastqsanger.gz | |||
| SRR23357702_1.fastq.gz | Fastqsanger.gz |
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Project description:Oxygen is a key signalling component of plant biology, and whilst an oxygen-sensing mechanism was previously described in Arabidopsis thaliana, key features of the associated PCO N-degron pathway and Group VII ETHYLENE RESPONSE FACTOR (ERFVII) transcription factor substrates remain unknown. We demonstrate that ERFVIIs show non-autonomous activation of root hypoxia tolerance, and are essential for root development and survival under oxygen limiting conditions in the soil. We determine the combined effects of ERFVIIs in controlling genome expression and define genetic and environmental components required for proteasome-dependent oxygen-regulated stability of ERFVIIs through the PCO N-degron pathway. Using a plant extract, unexpected amino-terminal cysteine sulphonic acid oxidation level of ERFVIIs was observed, suggesting a requirement for additional enzymatic activity within the pathway. Our results provide a holistic understanding of the properties, functions and readouts of this oxygen-sensing mechanism defined through its role in modulating ERFVII stability.
2023-07-03 | GSE224694 | GEO
Project description:Oxygen-sensing through ERFVII action and modulation in Arabidopsis thaliana
| PRJEB59551 | ENA
Project description:Oxygen is a key signalling component of plant biology and, whilst an oxygen-sensing mechanism was previously described in Arabidopsis thaliana. However, key features of the associated PCO N-degron pathway and Group VII ETHYLENE RESPONSE FACTOR (ERFVII) transcription factor substrates remain unknown. We demonstrate that ERFVIIs show non-autonomous activation of root hypoxia tolerance, and are essential for root development and survival under oxygen limiting conditions in the soil. We determine the combined effects of ERFVIIs in controlling genome expression and define genetic and environmental components required for proteasome-dependent oxygen-regulated stability of ERFVIIs through the PCO N-degron pathway. Using a plant extract, unexpected amino-terminal cysteine oxidation to sulphonic acid oxidation level of ERFVIIs was defined, suggesting a requirement for additional enzymatic activity within the pathway. Our results provide a holistic understanding of the properties, functions and readouts of this oxygen-sensing mechanism defined through its role in modulating ERFVII stability.
2023-07-02 | PXD039288 | Pride
Project description:Oxygen is a key signalling component of plant biology, and whilst an oxygen-sensing mechanism was previously described in Arabidopsis thaliana, key features of the associated PLANT CYSTEINE OXIDASE (PCO) N-degron pathway and Group VII ETHYLENE RESPONSE FACTOR (ERFVII) transcription factor substrates remain untested or unknown. We demonstrate that ERFVIIs show non-autonomous activation of root hypoxia tolerance and are essential for root development and survival under oxygen limiting conditions in soil. We determine the combined effects of ERFVIIs in controlling gene expression and define genetic and environmental components required for proteasome-dependent oxygen-regulated stability of ERFVIIs through the PCO N-degron pathway. Using a plant extract, unexpected amino-terminal cysteine sulphonic acid oxidation level of ERFVIIs was observed, suggesting a requirement for additional enzymatic activity within the pathway. Our results provide a holistic understanding of the properties, functions and readouts of this oxygen-sensing mechanism defined through its role in modulating ERFVII stability.
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Project description:This series compares the effects that two pharmacologically distinct ligands at the mitochondrial peripheral-type benzodiazepine receptor (Bzrp) has on gene expression in early mouse embryos cultured under different oxygen levels. Mouse embryos averaging 16-18 somite pairs were explanted on 9 d.p.c. and grown in culture under optimal oxygenation (21% oxygen, hyperbaric with respect to arterial blood = 80-100 mmHg). Most embryos (>90%) develop normally in over a 24h culture period. When embryos receive suboptimal oxygenation for 2.0h (5% oxygen, similar to venous blood = 38-40 mmHg) a high percentage of them (>60%) go on to develop abnormally or else fail. These hypoxic embryos are remediated with 5 uM PK11195 to ~25% malformation rate. Cultured embryos were exposed to different oxygen levels (5% or 21%) in the presence of the Bzrp ligands PK11195 (Bzrp antagonist) versus Ro5-4864 (Bzrp agonist). The sampling time was guided by p53 protein induction with hypoxia, and remediation with PK11195, at 4.0h of culture and exposures. Thus all measurements were on RNA from the prosencephalon collected 2.0h after start of the test period on 9 d.p.c. Keywords = peripheral benzodiazepine receptor Keywords = oxygen sensing Keywords = Bzrp ligands Keywords = PK11195 Keywords = Ro5-4864 Keywords = embryo Keywords = p53 protein induction
2010-06-09 | E-GEOD-1079 | biostudies-arrayexpress
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Project description:Osteocyte Egln1/Phd2 links oxygen sensing and biomineralization via FGF23
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Project description:Adaptation to low levels of O2 (hypoxia) is a universal biological feature across metazoans. Yet the underlying mechanisms how different species sense O2 deprivation remain to be deciphered. Here we functionally characterize a novel long non-coding RNA (lncRNA), LOC105369301, which we termed hypoxia-induced lncRNA for PLK1 stabilization or HILPS. HILPS exhibits appreciable basal expression exclusively in a broad range of human normal and cancer cells and is robustly induced by hypoxia inducible factor 1α (HIF1α). HILPS binds PLK1 and sequesters it from proteasome degradation. Stabilized PLK1 directly phosphorylates HIF1α and enhance its stability, constituting a positive feedforward circuit that reinforces oxygen sensing by HIF1α. HILPS inactivation triggers catastrophic adaptation defect during hypoxia in both normal and cancer cells. These findings introduce a mechanism that underlies the HIF1α identity deeply interconnected with PLK1 integrity, and identify the HILPS-PLK1-HIF1α pathway as a crucial oxygen-sensing axis in regulation of human physiological and pathogenic processes.
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Project description:The bone microenvironment is composed of niches that house cells across variable oxygen tensions. However, the contribution of oxygen gradients in regulating bone and blood homeostasis remains unknown. Here, we generated mice with either single or combined genetic inactivation of the critical oxygen-sensing prolyl hydroxylase (PHD) enzymes (PHD1-3) in osteoprogenitors. Hypoxia-inducible factor (HIF) activation associated with Phd2 and Phd3 inactivation drove bone accumulation by modulating osteoblastic/osteoclastic cross-talk through the direct regulation of osteoprotegerin (OPG). In contrast, combined inactivation of Phd1, Phd2, and Phd3 resulted in extreme HIF signaling, leading to polycythemia and excessive bone accumulation by overstimulating angiogenic-osteogenic coupling. We also demonstrate that genetic ablation of Phd2 and Phd3 was sufficient to protect ovariectomized mice against bone loss without disrupting hematopoietic homeostasis. Importantly, we identify OPG as a HIF target gene capable of directing osteoblast-mediated osteoclastogenesis to regulate bone homeostasis. Here, we show that coordinated activation of specific PHD isoforms fine-tunes the osteoblastic response to hypoxia, thereby directing two important aspects of bone physiology: cross-talk between osteoblasts and osteoclasts and angiogenic-osteogenic coupling.
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