Multi-omics profiling of living human pancreatic islet donors reveals heterogeneous beta cell trajectories toward type 2 diabetes
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA690574 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13380500.fastq.gz | Fastqsanger.gz | |||
| SRR13380501.fastq.gz | Fastqsanger.gz | |||
| SRR13380502.fastq.gz | Fastqsanger.gz | |||
| SRR13380503.fastq.gz | Fastqsanger.gz | |||
| SRR13380504.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 133 |
Similar Datasets
Project description:To gain insight into the history of islet cell deterioration along the progression from normal glycemic regulation to T2D, we collected surgical pancreatic tissue samples from 133 metabolically phenotyped pancreatectomized patients (PPP). Gene expression profiles of islets isolated by laser capture microdissection (LCM) from resected and snap-frozen pancreas samples were assessed by RNA sequencing.
2021-04-13 | GSE164416 | GEO
Project description:The cohesin complex shapes chromosomes by DNA loop extrusion, but individual extrusion trajectories were so far unappreciable in vivo. Here, we developed and validated TArgeted Cohesin Loader (TACL), a system enabling the strong activation of anchored loop extrusion from dozens of defined genomic sites in living cells. Studying their individual loop extrusion trajectories revealed that extruding cohesin-STAG2 stops not only at domain boundaries but at all flanking CTCF sites, engaging them in a complex transient looping network that supports intradomain contacts. Cohesin-STAG1 cannot associate with weak CTCF binding sites and fails to similarly support intradomain interactions. NIPBL-MAU2 remains associated with cohesin when stalled at looping CTCF sites, suggesting these factors may also be required for loop stabilization. TACL induces cohesin traffic jams and illegal loops with divergent CTCF sites, demonstrating that stalled cohesin can block extruding cohesin in vivo. Genes exposed to TACL-induced loop extrusion were collectively hindered in transcription and the underlying chromatin altered its accessibility and reduced its H3K27ac marks. Thus, by enabling the study of individual loop extrusion trajectories in vivo, we could assign new functions to players, identify new looping networks and uncover an interplay between loop extrusion, gene transcription and chromatin composition.
2025-06-26 | GSE278982 | GEO
Project description:The cohesin complex shapes chromosomes by DNA loop extrusion, but individual extrusion trajectories were so far unappreciable in vivo. Here, we developed and validated TArgeted Cohesin Loader (TACL), a system enabling the strong activation of anchored loop extrusion from dozens of defined genomic sites in living cells. Studying their individual loop extrusion trajectories revealed that extruding cohesin-STAG2 stops not only at domain boundaries but at all flanking CTCF sites, engaging them in a complex transient looping network that supports intradomain contacts. Cohesin-STAG1 cannot associate with weak CTCF binding sites and fails to similarly support intradomain interactions. NIPBL-MAU2 remains associated with cohesin when stalled at looping CTCF sites, suggesting these factors may also be required for loop stabilization. TACL induces cohesin traffic jams and illegal loops with divergent CTCF sites, demonstrating that stalled cohesin can block extruding cohesin in vivo. Genes exposed to TACL-induced loop extrusion were collectively hindered in transcription and the underlying chromatin altered its accessibility and reduced its H3K27ac marks. Thus, by enabling the study of individual loop extrusion trajectories in vivo, we could assign new functions to players, identify new looping networks and uncover an interplay between loop extrusion, gene transcription and chromatin composition.
2025-06-26 | GSE278397 | GEO
Project description:The cohesin complex shapes chromosomes by DNA loop extrusion, but individual extrusion trajectories were so far unappreciable in vivo. Here, we developed and validated TArgeted Cohesin Loader (TACL), a system enabling the strong activation of anchored loop extrusion from dozens of defined genomic sites in living cells. Studying their individual loop extrusion trajectories revealed that extruding cohesin-STAG2 stops not only at domain boundaries but at all flanking CTCF sites, engaging them in a complex transient looping network that supports intradomain contacts. Cohesin-STAG1 cannot associate with weak CTCF binding sites and fails to similarly support intradomain interactions. NIPBL-MAU2 remains associated with cohesin when stalled at looping CTCF sites, suggesting these factors may also be required for loop stabilization. TACL induces cohesin traffic jams and illegal loops with divergent CTCF sites, demonstrating that stalled cohesin can block extruding cohesin in vivo. Genes exposed to TACL-induced loop extrusion were collectively hindered in transcription and the underlying chromatin altered its accessibility and reduced its H3K27ac marks. Thus, by enabling the study of individual loop extrusion trajectories in vivo, we could assign new functions to players, identify new looping networks and uncover an interplay between loop extrusion, gene transcription and chromatin composition.
2025-06-26 | GSE278395 | GEO
Project description:The cohesin complex shapes chromosomes by DNA loop extrusion, but individual extrusion trajectories were so far unappreciable in vivo. Here, we developed and validated TArgeted Cohesin Loader (TACL), a system enabling the strong activation of anchored loop extrusion from dozens of defined genomic sites in living cells. Studying their individual loop extrusion trajectories revealed that extruding cohesin-STAG2 stops not only at domain boundaries but at all flanking CTCF sites, engaging them in a complex transient looping network that supports intradomain contacts. Cohesin-STAG1 cannot associate with weak CTCF binding sites and fails to similarly support intradomain interactions. NIPBL-MAU2 remains associated with cohesin when stalled at looping CTCF sites, suggesting these factors may also be required for loop stabilization. TACL induces cohesin traffic jams and illegal loops with divergent CTCF sites, demonstrating that stalled cohesin can block extruding cohesin in vivo. Genes exposed to TACL-induced loop extrusion were collectively hindered in transcription and the underlying chromatin altered its accessibility and reduced its H3K27ac marks. Thus, by enabling the study of individual loop extrusion trajectories in vivo, we could assign new functions to players, identify new looping networks and uncover an interplay between loop extrusion, gene transcription and chromatin composition.
2025-06-26 | GSE281421 | GEO
Project description:The cohesin complex shapes chromosomes by DNA loop extrusion, but individual extrusion trajectories were so far unappreciable in vivo. Here, we developed and validated TArgeted Cohesin Loader (TACL), a system enabling the strong activation of anchored loop extrusion from dozens of defined genomic sites in living cells. Studying their individual loop extrusion trajectories revealed that extruding cohesin-STAG2 stops not only at domain boundaries but at all flanking CTCF sites, engaging them in a complex transient looping network that supports intradomain contacts. Cohesin-STAG1 cannot associate with weak CTCF binding sites and fails to similarly support intradomain interactions. NIPBL-MAU2 remains associated with cohesin when stalled at looping CTCF sites, suggesting these factors may also be required for loop stabilization. TACL induces cohesin traffic jams and illegal loops with divergent CTCF sites, demonstrating that stalled cohesin can block extruding cohesin in vivo. Genes exposed to TACL-induced loop extrusion were collectively hindered in transcription and the underlying chromatin altered its accessibility and reduced its H3K27ac marks. Thus, by enabling the study of individual loop extrusion trajectories in vivo, we could assign new functions to players, identify new looping networks and uncover an interplay between loop extrusion, gene transcription and chromatin composition.
2025-06-26 | GSE277608 | GEO
Project description:The objective of the study was to characterize the immunoreactivity profiles of IgG-reactive epitopes in COVID-19 patients with distinct disease trajectories as well as SARS-CoV-2-naïve sera, using a high-density SARS-CoV-2 whole proteome peptide microarray. The microarray comprised of a total of 5347 individual peptides, each consisting of 15 amino acids with an overlap of 13 amino acids printed in duplicate. The microarray also had a panel of the most relevant mutations from SARS-CoV-2 variants of concern like omicron, alpha, beta, gamma, delta, and others. This study consisted of 29 participants, including 10 naïve controls (5 pre-pandemic and 5 SARS-CoV-2 seronegative) and 19 RT-PCR-confirmed COVID-19 patients. The COVID-19 patients were stratified into two distinct cohorts based on their disease trajectories: the severe cohort (S), in which the patients presented moderate COVID-19 symptoms initially but eventually progressed toward severity; and the recovered cohort (R), in which severe COVID-19 patients progressed toward recovery. Our findings contribute to a deeper understanding of the immunopathogenesis of COVID-19 in patients with different disease trajectories, the effect of mutations on immunoreactivity, and potential cross-reactivity due to exposure to common cold viruses.
2025-03-31 | E-MTAB-14495 | biostudies-arrayexpress
Project description:The epiblast of vertebrate embryos is comprised of neural and non-neural ectoderm, with the border territory at their intersection harbouring neural crest and cranial placode progenitors. Here we profile avian epiblast cells as a function of time using single-cell RNA-seq to define transcriptional changes in the emerging ‘neural plate border’. The results reveal gradual establishment of heterogeneous neural plate border signatures, including novel genes that we validate by fluorescent in situ hybridization. Developmental trajectory analysis shows that segregation of neural plate border lineages only commences at early neurulation, rather than at gastrulation as previously predicted. We find that cells expressing the prospective neural crest marker Pax7 contribute to multiple lineages, and a subset of premigratory neural crest cells shares a transcriptional signature with their border precursors. Together, our results suggest that cells at the neural plate border remain heterogeneous until early neurulation, at which time progenitors become progressively allocated toward defined lineages.
2021-12-31 | GSE181577 | GEO
Project description:Characterization of induced cohesin loop extrusion trajectories in living cells
| PRJNA905468 | ENA
Project description:Segregation of neural crest specific lineage trajectories from a heterogeneous neural plate border territory only emerges at neurulation
| PRJNA752590 | ENA