EVG1 regulates vascular development and regeneration in response to stress
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA931753 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23343805_1.fastq.gz | Fastqsanger.gz | |||
| SRR23343805_2.fastq.gz | Fastqsanger.gz | |||
| SRR23343806_1.fastq.gz | Fastqsanger.gz | |||
| SRR23343806_2.fastq.gz | Fastqsanger.gz | |||
| SRR23343807_1.fastq.gz | Fastqsanger.gz |
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Project description:Vascular tissues possess remarkable regenerative abilities, quickly healing post damage from wounding, grafting, or drought. The regenerative ability is also relevant for many plant pathogens that invade host tissues and induce the formation of vasculature to derive nutrients, thereby suggesting a possible mechanistic overlap in vascular regeneration between stresses. With comparative transcriptomics we identified a gene that was highly upregulated in Agrobacterium infection, nematode infection, and during graft formation. Loss of function mutant of EVG1 enhanced ectopic xylem formation in Vascular cell Induction culture System Using Arabidopsis Leaves (VISUAL) and enhanced graft formation and was termed ENHANCER OF VISUAL AND GRAFTING 1 (EVG1). EVG1 promoted cambium development and inhibited vascular regeneration during grafting. Transcriptomic analyses found that stress responsive, cell wall related, and ABA response related genes were differentially expressed in evg1. Mutants of EVG1 also phenocopied mutants of RLP44, a receptor that interacts with the receptors of both the brassinosteroid (BR) and phytosulfokine (PSK) signaling pathway to incorporate cell wall damages cues into hormone signaling and help maintain procambium cell identity. We identified that EVG1 is highly stress responsive while RLP44 is not despite showing similar phenotypes in developmental assays. We propose that EVG1 and RLP44 act in the same pathway. EVG1 might act as a stress signal and regulates development while indirectly also influencing the RLP44 associated pathways.
2025-01-09 | GSE224565 | GEO
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Project description:Regeneration is a common strategy for plants to repair their damaged body plans after attack from other organisms or physical assaults. Trees with bark girdling on a large scale will grow new bark within one month and this bark regeneration after girdling system has been proven to be an efficient method to study secondary vascular development as well as plant tissue regeneration in vivo. We herein show the molecular features of differentiating xylem cell fate switch process during secondary vascular tissue (SVT) regeneration in Populus. Based on our data, we propose a working model to illustrate the molecular dynamics underlying xylem cell fate switch process during SVT regeneration, which is significant to understand the pattern formation during the SVTs regeneration and also would shed light on the mechanisms of tissue regeneration in plants. Specific regenerated tissues of Populus at different stages were isolated by tangential cryo-sectioning. Total RNA from cryo-sections representing different regenerating tissues was extracted for Affymetrix Poplar Whole Genome Array hybridization. Five samples (two replicates for each sample) were used for gene expression analysis: differentiating xylem (diX, Stage 0), dedifferentiating xylem cells (deX, Stage I), regenerated phloem (rPh, Stage II), differentiating regenerated cambium (diC, Stage II) and regenerated cambium (rC, Stage III). In addition, one pooled genomic DNA sample from cryo-sections of differentiating xylem from two trees was isolated for DNA hybridization to produce a new CDF file that was used to mask out some potentially cross-hybridizing probesets from the standard Affymetrix Poplar Genome Array. Supplementary file: poplar.cdf
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Project description:This SuperSeries is composed of the following subset Series: GSE32709: DNA methylation regulates lineage-specifying genes in the human vascular system [expression array]. GSE34486: DNA methylation regulates lineage-specifying genes in the human vascular system [methylation array]. Refer to individual Series
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Project description:Regeneration is a common strategy for plants to repair their damaged body plans after attack from other organisms or physical assaults. Trees with bark girdling on a large scale will grow new bark within one month and this bark regeneration after girdling system has been proven to be an efficient method to study secondary vascular development as well as plant tissue regeneration in vivo. We herein show the molecular features of differentiating xylem cell fate switch process during secondary vascular tissue (SVT) regeneration in Populus. Based on our data, we propose a working model to illustrate the molecular dynamics underlying xylem cell fate switch process during SVT regeneration, which is significant to understand the pattern formation during the SVTs regeneration and also would shed light on the mechanisms of tissue regeneration in plants.
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Project description:<p>Acute kidney injury (AKI) is a known risk factor for the development of chronic kidney disease (CKD), with no satisfactory strategy to prevent the progression of AKI to CKD. Damage to the renal vascular system and subsequent hypoxia are common contributors to both AKI and CKD. Hypoxia inducible factor (HIF) is reported to protect the kidney from acute ischemic damage and a novel HIF stabilizer, FG4592 (Roxadustat), has become available in the clinic as an anti-anemia drug. However, the role of FG4592 in the AKI-to-CKD transition remains elusive. In the present study, we investigated the role of FG4592 in the AKI-to-CKD transition induced by unilateral kidney ischemia-reperfusion (UIR). The results showed that FG4592, given to mice 3 days after UIR, markedly alleviated kidney fibrosis and enhanced renal vascular regeneration, possibly via activating the HIF-1α/vascular endothelial growth factor A (VEGFA)/VEGF receptor 1 (VEGFR1) signaling pathway and driving the expression of the endogenous antioxidant superoxide dismutase 2 (SOD2). In accordance with the improved renal vascular regeneration and redox balance, the metabolic disorders of the UIR mice kidneys were also attenuated by treatment with FG4592. However, the inflammatory response in the UIR kidneys was not affected significantly by FG-4592. Importantly, in the kidneys of CKD patients, we also observed enhanced HIF-1α expression which was positively correlated with the renal levels of VEGFA and SOD2. Together, these findings demonstrated the therapeutic effect of the anti-anemia drug FG-4592 in preventing the AKI-to-CKD transition related to ischemia and the redox imbalance.</p><p><br></p><p>Linked study:</p><p><strong>UPLC-MS assay</strong> of mice kidney tissue sacrificed at<strong> day 10 </strong>after UIR is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS3056' rel='noopener noreferrer' target='_blank'>MTBLS3056</a></p>
2021-07-22 | MTBLS3003 | MetaboLights
Project description:<p>Acute kidney injury (AKI) is a known risk factor for the development of chronic kidney disease (CKD), with no satisfactory strategy to prevent the progression of AKI to CKD. Damage to the renal vascular system and subsequent hypoxia are common contributors to both AKI and CKD. Hypoxia inducible factor (HIF) is reported to protect the kidney from acute ischemic damage and a novel HIF stabilizer, FG4592 (Roxadustat), has become available in the clinic as an anti-anemia drug. However, the role of FG4592 in the AKI-to-CKD transition remains elusive. In the present study, we investigated the role of FG4592 in the AKI-to-CKD transition induced by unilateral kidney ischemia-reperfusion (UIR). The results showed that FG4592, given to mice 3 days after UIR, markedly alleviated kidney fibrosis and enhanced renal vascular regeneration, possibly via activating the HIF-1α/vascular endothelial growth factor A (VEGFA)/VEGF receptor 1 (VEGFR1) signaling pathway and driving the expression of the endogenous antioxidant superoxide dismutase 2 (SOD2). In accordance with the improved renal vascular regeneration and redox balance, the metabolic disorders of the UIR mice kidneys were also attenuated by treatment with FG4592. However, the inflammatory response in the UIR kidneys was not affected significantly by FG-4592. Importantly, in the kidneys of CKD patients, we also observed enhanced HIF-1α expression which was positively correlated with the renal levels of VEGFA and SOD2. Together, these findings demonstrated the therapeutic effect of the anti-anemia drug FG-4592 in preventing the AKI-to-CKD transition related to ischemia and the redox imbalance.</p><p><br></p><p>Linked study:</p><p><strong>UPLC-MS assay</strong> of mice kidney tissues sacrificed at <strong>day 21 </strong>after UIR is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS3003' rel='noopener noreferrer' target='_blank'>MTBLS3003</a></p>
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Project description:The periosteum contains a highly osteogenic and neuro-vascular microenvironment that is essential for cortical bone formation and regeneration. Resident tissue macrophages (RTMs) are critical for maintaining tissue-specific niches and participating in tissue regeneration. However, the characteristics, origin and functions of periosteum-resident macrophages (PRMs) remain largely unknown. In this study, we demonstrated that PRMs are generated during embryonic hematopoiesis and are self-maintained locally during regeneration. Furthermore, by single-cell RNA sequencing analysis of periosteum myeloid cells, CX3CR1+CD45+ACE+ and CX3CR1+CD45+CD74+ cells were identified as vascular-associated and neuro-associated PRMs, respectively. Both cell types were found to arise from CX3CR1+CD168+CD45+ PRMs and shown to play critical roles in maintaining the periosteum neuro-vascular niche and promoting early-stage cortical bone regeneration. Importantly, the neuro-vascular characteristic of PRMs are directly modulated via Periostin, the essential ECM distributed in periosteum. These findings elucidate the characteristics and origins of PRMs and reveal their essential roles in maintaining the local niche and cortical bone regeneration as well as highlighting the potential value of PRMs as a therapeutic target in bone regeneration.
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