Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1126448 | ENA |
REPOSITORIES: ENA
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Project description:Dynamics in zebrafish development define transcriptomic specificity after angiogenesis inhibitor exposure (SU4312)
| PRJNA1126151 | ENA
Project description:Time-series transcriptomic data of ZFE exposed to the angiogenesis inhibitor SU4312 with exposure start time points at 0 hpf and 24 hpf.
2025-01-09 | GSE270785 | GEO
Project description:Time-series transcriptomic data of ZFE exposed to the angiogenesis inhibitor SU4312 with exposure start time points at 0 hpf and 24 hpf.
2025-01-09 | GSE270294 | GEO
Project description:The ribosome is a translational apparatus that comprises about 80 ribosomal proteins and four rRNAs. Recent studies reported that ubiquitination of the ribosomal proteins plays a pivotal role in translational control and ribosome-associated quality control (RQC). However, little is known about the dynamics of ribosome ubiquitination under complex biological processes of multicellular organisms. To study ribosome ubiquitination during animal development, we generated a zebrafish strain that expresses a FLAG-tagged ribosomal protein Rpl36/eL36 from its endogenous locus. Combining affinity purification of ribosomes from rpl36-FLAG zebrafish embryos with immunoblotting analysis, we analyzed ribosome ubiquitination during zebrafish development. Our data showed that ubiquitination of ribosomal proteins dynamically changed as development proceeded. We further revealed that Znf598, an E3 ubiquitin ligase that triggers RQC, contributed to the ribosome ubiquitination during zebrafish development. LC-MS/MS analysis and immunoblotting analysis identified lysines 139 of ribosomal protein Rps10/eS10 as pivotal ubiquitination sites on the ribosome during development. Finally, we demonstrated that an Rps10 K139/140R mutation reduced overall ribosome ubiquitination pattern. Collectively, these results reveal dynamics and complexity of ribosome ubiquitination in zebrafish development.
2023-10-11 | PXD039560 | JPOST Repository
Project description:Through deep sequencing and functional screening in zebrafish, we find that miR-221 is essential for angiogenesis. miR-221 knockdown phenocopied defects associated with loss of the tip cell-expressed Flt4 receptor. Furthermore, miR-221 was required for tip cell proliferation and migration, as well as tip cell potential in mosaic blood vessels. miR-221 knockdown also prevented “hyper-angiogenesis” defects associated with Notch deficiency and miR-221 expression was inhibited by Notch signaling. Finally, miR-221 promoted tip cell behavior through repression of two targets: cyclin-dependent kinase inhibitor 1b (cdkn1b) and phosphoinositide-3-kinase regulatory subunit 1 (pik3r1). These results identify miR-221 as an important regulatory node through which tip cell migration and proliferation are controlled during angiogenesis. Identification of endothelial-expressed microRNA from FACS-isolated zebrafish endothelial cells.
2012-02-28 | E-GEOD-35078 | biostudies-arrayexpress
Project description:Trichloroethylene (TCE) is primarily used as an industrial degreasing agent and has been in use since the 1940s. TCE is released into the soil, surface, and groundwater. From an environmental and regulatory standpoint more than half of Superfund hazardous waste sites on the National Priority List are contaminated with TCE. Occupational exposure to TCE occurs primarily via inhalation, while environmental TCE exposure also occurs through ingestion of contaminated drinking water. Current literature links TCE exposure to various adverse health effects including cardiovascular toxicity. Current studies aiming to address developmental cardiovascular toxicity utilized rodent and avian models with the majority of studies using relatively higher parts per million (ppm; mg/L) doses. In this study to further investigate developmental cardiotoxicity of TCE, zebrafish embryos were treated with 0, 10, 100, or 500 parts per billion (ppb; μg/L) TCE during embryogenesis and/or through early larval stages. After the appropriate exposure period, angiogenesis, F-actin polymerization, and mitochondrial function were assessed. A significant dose response decrease in angiogenesis, F-actin polymerization, and mitochondrial function was observed. To further complement this data, a transcriptomic profile of zebrafish larvae was completed to identify gene alterations associated with the 10 ppb TCE exposure. Results from the transcriptomic data revealed that an embryonic TCE exposure caused significant changes in genes associated with cardiovascular disease, cancer, and organismal injury and abnormalities with a number of targets in the FAK signaling pathway. Overall, results from our study further support TCE as a developmental cardiovascular toxicant and continued priority for environmental regulation.
2016-02-01 | GSE72918 | GEO
Project description:Signaling events that regulate central nervous system (CNS) angiogenesis and blood-brain barrier (BBB) formation are only beginning to be elucidated. By evaluating the gene expression profile of mouse vasculature, we identified DR6/TNFRSF21 and TROY/TNFRSF19 as regulators of CNS-specific angiogenesis in both zebrafish and mice. Furthermore, these two death receptors interact both genetically and physically and are required for vascular endothelial growth factor (VEGF)-mediated JNK activation and subsequent human brain endothelial sprouting in vitro. Increasing beta-catenin levels in brain endothelium upregulate DR6 and TROY, indicating that these death receptors are downstream target genes of Wnt/beta-catenin signaling, which has been shown to be required for BBB development. These findings define a role for death receptors DR6 and TROY in CNS-specific vascular development. 5 replicates of 3 time points for either brain or liver/lung facs sorted vascaulture. One adult liver/lung replicate was not used as it failed QC
2012-02-15 | E-GEOD-35802 | biostudies-arrayexpress
Project description:Chronic early life stress can affect development of the neuroendocrine stress system, leading to its persistent dysregulation and consequently increased disease risk in adulthood. One contributing factor is thought to be epigenetic programming in response to chronic glucocorticoid exposure during early development. We have previously shown that zebrafish embryos treated chronically with cortisol develop into adults with constitutively elevated whole body cortisol and aberrant immune gene expression. The objective of the experiments reported here was to further characterize the phenotype of those adults. We find that adult zebrafish derived from cortisol-treated embryos have aberrant cortisol tissue distribution and dynamics, which correlate with differential transcriptional activity of key glucocorticoid-responsive regulatory genes klf9 and fkbp5 in blood and brain.
2019-10-28 | GSE137987 | GEO
Project description:The core-promoter, a stretch of DNA surrounding the transcription-start-site (TSS), is a major integration-point for regulatory-signals controlling gene-transcription. Cellular-differentiation is marked by divergence in transcriptional-repertoire and cell- cycling behaviour between cells of different fates. The role promoter-associated gene- regulatory-networks play in development-associated transitions in cell-cycle- dynamics is poorly understood. This study demonstrates in a vertebrate embryo, how core-promoter variations define transcriptional-output in cells transitioning from a proliferative to cell-lineage specifying phenotype. Assessment of cell-proliferation across zebrafish embryo-development, using the FUCCI-transgenic cell-cycle- phase marker, revealed a spatial and lineage-specific separation in cell-cycling behaviour. To investigate the role differential promoter-usage plays in this process, cap-analysis-of-gene-expression (CAGE) was performed on cells segregated by cycling-dynamics.
2020-06-19 | E-MTAB-8795 | biostudies-arrayexpress