Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10759694_1.fastq.gz | Fastqsanger.gz | |||
| SRR10759694_2.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Polyethylene pollutions are considered inert in nature and adversely affect the entire ecosystem. Larvae of greater wax moths (Galleria mellonella) have the ability to masticate and potentially biodegrade polyethylene films at elevated rates. The wax moth has been thought to metabolize PE independently of gut flora, however, the role of the microbiome is poorly understood and degradation by the wax moth might be involved. To determine whether the salivary glands of the wax moth were potentially involved in the PE degradation, it was investigated how surface changes of polyethylene were affected by mastication and consumption. Formation of pitting and degradation intermediates, including carbonyl groups, indicated that salivary glands could assist in polyethylene metabolism. We investigated the biochemical effect of exposure to PE on the composition of the salivary gland proteome. The expression of salivary proteins was found to be affected by PE exposure. The proteins that were significantly affected by the exposure to PE revealed that the wax moth is undergoing general changes in energy levels, and that enzymatic pathways associated with fatty acid beta oxidation were induced during PE consumption.
2020-03-19 | PXD016834 | Pride
Project description:In primed human pluripotent stem cells (hPSCs) resembling post-implantation epiblast, numerous lineage-specific enhancers assume the poised chromatin state, co-marked by H3K4me1 and Polycomb-associated H3K27me3 histone modifications. In contrast, these poised enhancers (PEs) are scarce in naive hPSCs that model pre-implantation epiblast. PEs form abundant chromosomal contacts with developmental genes, but when these contacts emerge, how their formation relates to enhancer poising and their functional significance remains incompletely understood. Here, we devise high-resolution, PE-targeted Capture Hi-C to generate a comprehensive atlas of PE chromosomal contacts in the time course of hPSC transition from the naive to primed state. We find that enhancer poising emerges early in the transition, while the contacts show diverse dynamics that is only partially coupled to poising. PROTAC-induced degradation of Polycomb Repressive Complex 2 (PRC2) early in the transition weakens PE connectivity, while inhibition of its H3K27 methyltransferase activity does not, suggesting a non-catalytic role of Polycomb in supporting PE contacts. Notably, PE contacts persist after developmental activation or ectopic CRISPRa targeting and can mediate long-range gene induction. Together, these findings reveal the temporal and mechanistic principles of PE connectivity, highlighting a potential role of PE contacts in establishing gene expression patterns in human development.
2026-06-08 | GSE309055 | GEO
Project description:In primed human pluripotent stem cells (hPSCs) resembling post-implantation epiblast, numerous lineage-specific enhancers assume the poised chromatin state, co-marked by H3K4me1 and Polycomb-associated H3K27me3 histone modifications. In contrast, these poised enhancers (PEs) are scarce in naive hPSCs that model pre-implantation epiblast. PEs form abundant chromosomal contacts with developmental genes, but when these contacts emerge, how their formation relates to enhancer poising and their functional significance remains incompletely understood. Here, we devise high-resolution, PE-targeted Capture Hi-C to generate a comprehensive atlas of PE chromosomal contacts in the time course of hPSC transition from the naive to primed state. We find that enhancer poising emerges early in the transition, while the contacts show diverse dynamics that is only partially coupled to poising. PROTAC-induced degradation of Polycomb Repressive Complex 2 (PRC2) early in the transition weakens PE connectivity, while inhibition of its H3K27 methyltransferase activity does not, suggesting a non-catalytic role of Polycomb in supporting PE contacts. Notably, PE contacts persist after developmental activation or ectopic CRISPRa targeting and can mediate long-range gene induction. Together, these findings reveal the temporal and mechanistic principles of PE connectivity, highlighting a potential role of PE contacts in establishing gene expression patterns in human development.
2026-06-08 | GSE309054 | GEO
Project description:In primed human pluripotent stem cells (hPSCs) resembling post-implantation epiblast, numerous lineage-specific enhancers assume the poised chromatin state, co-marked by H3K4me1 and Polycomb-associated H3K27me3 histone modifications. In contrast, these poised enhancers (PEs) are scarce in naive hPSCs that model pre-implantation epiblast. PEs form abundant chromosomal contacts with developmental genes, but when these contacts emerge, how their formation relates to enhancer poising and their functional significance remains incompletely understood. Here, we devise high-resolution, PE-targeted Capture Hi-C to generate a comprehensive atlas of PE chromosomal contacts in the time course of hPSC transition from the naive to primed state. We find that enhancer poising emerges early in the transition, while the contacts show diverse dynamics that is only partially coupled to poising. PROTAC-induced degradation of Polycomb Repressive Complex 2 (PRC2) early in the transition weakens PE connectivity, while inhibition of its H3K27 methyltransferase activity does not, suggesting a non-catalytic role of Polycomb in supporting PE contacts. Notably, PE contacts persist after developmental activation or ectopic CRISPRa targeting and can mediate long-range gene induction. Together, these findings reveal the temporal and mechanistic principles of PE connectivity, highlighting a potential role of PE contacts in establishing gene expression patterns in human development.
2026-06-08 | GSE309124 | GEO
Project description:Dysregulated expression of oncogenic splicing factors (SFs) occurs in human tumors in part through alterations in splicing of poison exons (PE), highly conserved exons that trigger RNA degradation. TRA2β is one such SF that undergoes PE suppression in tumor cells. Therefore, manipulation of TRA2β-PE can be a promising therapeutic strategy for cancer. Here, we demonstrate that low TRA2β-PE inclusion correlates with decreased patient survival across multiple tumor types. TRA2β-PE-targeting antisense oligonucleotides (ASOs) induce anti-cancer phenotypes and widespread transcriptomic alterations in cell culture models by causing both TRA2β protein knockdown and upregulation of TRA2β-PE-containing transcripts, which act as long-noncoding RNAs (lncRNAs) to sequester nuclear proteins. Finally, we demonstrate efficacy of TRA2β-PE-targeting ASOs in preclinical 3D organoid and in vivo patient-derived xenograft models. Together, this demonstrates that oncogenic SFs can be drugged using PE-targeting ASOs and elucidates a mechanism by which the TRA2β-PE acts both as a regulator of TRA2β protein expression and as a lncRNA that controls cancer cell growth.
2024-12-20 | PXD042941 | Pride
Project description:The study aimed to explore the potential of bacterial biodegradation as a solution to the global problem of plastic pollution, specifically targeting polyethylene (PE), one of the most common types of plastic. The goals of the study were to isolate a bacterial strain capable of breaking down PE, identify the key enzymes responsible for the degradation process, and understand the metabolic pathways involved.
2023-10-24 | PXD044483 | Pride
Project description:In primed human pluripotent stem cells (hPSCs) resembling post-implantation epiblast, numerous lineage-specific enhancers assume the poised chromatin state, co-marked by H3K4me1 and Polycomb-associated H3K27me3 histone modifications. In contrast, these poised enhancers (PEs) are scarce in naive hPSCs that model pre-implantation epiblast. PEs form abundant chromosomal contacts with developmental genes, but when these contacts emerge, how their formation relates to enhancer poising and their functional significance remains incompletely understood. Here, we devise high-resolution, PE-targeted Capture Hi-C to generate a comprehensive atlas of PE chromosomal contacts in the time course of hPSC transition from the naive to primed state. We find that enhancer poising emerges early in the transition, while the contacts show diverse dynamics that is only partially coupled to poising. PROTAC-induced degradation of Polycomb Repressive Complex 2 (PRC2) early in the transition weakens PE connectivity, while inhibition of its H3K27 methyltransferase activity does not, suggesting a non-catalytic role of Polycomb in supporting PE contacts. Notably, PE contacts persist after developmental activation or ectopic CRISPRa targeting and can mediate long-range gene induction. Together, these findings reveal the temporal and mechanistic principles of PE connectivity, highlighting a potential role of PE contacts in establishing gene expression patterns in human development.
2026-06-08 | GSE309123 | GEO
Project description:In primed human pluripotent stem cells (hPSCs) resembling post-implantation epiblast, numerous lineage-specific enhancers assume the poised chromatin state, co-marked by H3K4me1 and Polycomb-associated H3K27me3 histone modifications. In contrast, these poised enhancers (PEs) are scarce in naive hPSCs that model pre-implantation epiblast. PEs form abundant chromosomal contacts with developmental genes, but when these contacts emerge, how their formation relates to enhancer poising and their functional significance remains incompletely understood. Here, we devise high-resolution, PE-targeted Capture Hi-C to generate a comprehensive atlas of PE chromosomal contacts in the time course of hPSC transition from the naive to primed state. In this experiment, we show that PROTAC-induced degradation of Polycomb Repressive Complex 2 (PRC2) early in the transition weakens PE connectivity, while inhibition of its H3K27 methyltransferase activity does not, suggesting a non-catalytic role of Polycomb in supporting PE contacts.
2026-06-10 | GSE309649 | GEO
Project description:Autophagy is a conserved intracellular degradation pathway exerting various cytoprotective and homeostatic functions by utilizing de novo double membrane vesicle (autophagosome) formation to target a wide range of cytoplasmic material for vacuolar/lysosomal degradation. The Atg1 kinase is one of its key regulators coordinating a complex signaling program to orchestrate autophagosome formation. Combining in vitro reconstitution and cell based approaches, we demonstrate that Atg1 is activated by lipidated Atg8 (Atg8-PE) stimulating substrate phosphorylation along the growing autophagosomal membrane. Atg1 dependent phosphorylation of Atg13 triggers Atg1 complex dissociation resulting in rapid turnover of Atg1 complex subunits at the pre-autophagosomal structure. Moreover, Atg1 recruitment by Atg8-PE self-regulates Atg8-PE levels in the growing autophagosomal membrane by phosphorylating and inhibiting the Atg8 specific E2 and E3. Taken together, our work uncovers the molecular basis for positive and negative feedback imposed by Atg1, and opposing phosphorylation and dephosphorylation events governing the spatiotemporal regulation of autophagy.
2021-10-11 | PXD029047 | Pride
Project description:Preeclampsia (PE), a multifactorial pregnancy-specific syndrome accounting for up to 8% of pregnancy complications, is a leading cause of maternal and fetal morbidity and mortality and PE is also associated with long-term risk of hypertension and stroke for both the mother and fetus. Currently, the only “cure” is delivery of the baby and placenta, largely because the pathogenesis of preeclampsia is not yet fully understood. Preeclampsia is associated with impaired vascular remodeling at the maternal-fetal interface and placental insufficiency; however, the specific factors that contribute to this impairment have not been identified. To identify potential contributing pathways, we examined temporal transcriptomic changes occurring within the uterus, uterine implantation sites, and placentae from the Dahl salt-sensitive (Dahl S) rat model of superimposed preeclampsia compared to Sprague Dawley (SD) rats. We hypothesized that the Dahl S maternal-fetal interface would exhibit a unique temporal transcriptomic profile unveiling novel biomarkers, therapeutic targets, and mechanistic pathways regarding the development of PE. Our initial study focused on evaluation of genes previously linked to the development PE from using real time quantitative PCR (RT qPCR) and total RNA was isolated from uterus (day 0), uterine implantation sites (days 7, 10, 14), and placenta (days 14 and 20). Subsequently, an unbiased transcriptome analysis was performed at each time point using whole genome microarray to identify novel factors involved in PE. 624, 332, 185 , and 366 genes were found to be differentially expressed on days 0, 7, 10 and 14 respectively, with a Reactome Pathway enrichment for “Fatty acid metabolism, Metabolism of water-soluble vitamins and cofactors, Metabolism, Synthesis of substrates in N-glucan biosynthesis on Day 7”; ”Glycerophospholipid biosynthesis, Phospholipid metabolism, and Metabolism of lipids on Day 10”; and “Metabolism of lipids, Phospholipid metabolism, degradation of the extracellular matrix, Fatty acid metabolism, and Collagen degradation on Day 14” in the Dahl S rat vs. SD. Our data revealed numerous pathways that may play a role in the pathophysiology of spontaneous superimposed PE and allow for further investigation of novel therapeutic targets and biomarker development.
2019-09-10 | GSE130102 | GEO