Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Pancreatic Beta Cell Enhancers Regulate Rhythmic Transcription of Exocyst Triggering and Diabetes

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE70961 | GEO | 2015/11/10

SECONDARY ACCESSION(S): PRJNA290020

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Pancreatic Beta Cell Enhancers Regulate Rhythmic Transcription of Exocyst Triggering and Diabetes

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-11-10 | E-GEOD-70961 | biostudies-arrayexpress

Pancreatic Beta-Cell Enhancers Regulate Rhythmic Transcription of Exocyst Triggering and Diabetes [ChIP-seq]

Project description:The molecular clock is a transcriptional oscillator present in brain and peripheral cells that coordinates behavior and physiology with the solar cycle. Here we reveal that the clock gates insulin secretion through genome-wide transcriptional control of the pancreatic exocyst across species. Clock transcription factors bind to unique enhancer sites in cycling genes in beta cells that diverge from those in liver, revealing the dynamics of inter-tissue clock control of genomic and physiologic processes important in glucose homeostasis. ChIP-Seq in Beta-TC6 mouse beta cells

2015-11-10 | E-GEOD-70960 | biostudies-arrayexpress

Pancreatic Beta-Cell Enhancers Regulate Rhythmic Transcription of Exocyst Triggering and Diabetes [ChIP-seq]

2015-11-10 | GSE70960 | GEO

Pancreatic β cell enhancers regulate rhythmic transcription of genes controlling insulin secretion.

Project description:The mammalian transcription factors CLOCK and BMAL1 are essential components of the molecular clock that coordinate behavior and metabolism with the solar cycle. Genetic or environmental perturbation of circadian cycles contributes to metabolic disorders including type 2 diabetes. To study the impact of the cell-autonomous clock on pancreatic β cell function, we examined pancreatic islets from mice with either intact or disrupted BMAL1 expression both throughout life and limited to adulthood. We found pronounced oscillation of insulin secretion that was synchronized with the expression of genes encoding secretory machinery and signaling factors that regulate insulin release. CLOCK/BMAL1 colocalized with the pancreatic transcription factor PDX1 within active enhancers distinct from those controlling rhythmic metabolic gene networks in liver. We also found that β cell clock ablation in adult mice caused severe glucose intolerance. Thus, cell type-specific enhancers underlie the circadian control of peripheral metabolism throughout life and may help to explain its dysregulation in diabetes.

| S-EPMC4669216 | biostudies-literature

The microRNA-200 family regulates pancreatic beta-cell survival in type 2 diabetes

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-05-06 | E-GEOD-58505 | biostudies-arrayexpress

Circadian enhancers coordinate multiple phases of rhythmic gene transcription in vivo.

Project description:Mammalian transcriptomes display complex circadian rhythms with multiple phases of gene expression that cannot be accounted for by current models of the molecular clock. We have determined the underlying mechanisms by measuring nascent RNA transcription around the clock in mouse liver. Unbiased examination of enhancer RNAs (eRNAs) that cluster in specific circadian phases identified functional enhancers driven by distinct transcription factors (TFs). We further identify on a global scale the components of the TF cistromes that function to orchestrate circadian gene expression. Integrated genomic analyses also revealed mechanisms by which a single circadian factor controls opposing transcriptional phases. These findings shed light on the diversity and specificity of TF function in the generation of multiple phases of circadian gene transcription in a mammalian organ.

| S-EPMC4243056 | biostudies-literature

Pancreatic Islet Transcriptional Enhancers and Diabetes.

Project description:PURPOSE OF REVIEW:Common genetic variants that associate with type 2 diabetes risk are markedly enriched in pancreatic islet transcriptional enhancers. This review discusses current advances in the annotation of islet enhancer variants and their target genes. RECENT FINDINGS:Recent methodological advances now allow genetic and functional mapping of diabetes causal variants at unprecedented resolution. Mapping of enhancer-promoter interactions in human islets has provided a unique appreciation of the complexity of islet gene regulatory processes and enabled direct association of noncoding diabetes risk variants to their target genes. The recently improved human islet enhancer annotations constitute a framework for the interpretation of diabetes genetic signals in the context of pancreatic islet gene regulation. In the future, integration of existing and yet to come regulatory maps with genetic fine-mapping efforts and in-depth functional characterization will foster the discovery of novel diabetes molecular risk mechanisms.

| S-EPMC6872509 | biostudies-literature

The microRNA-200 family regulates pancreatic beta-cell survival in type 2 diabetes

Project description:This SuperSeries is composed of the SubSeries listed below.

2015-05-06 | GSE58505 | GEO

The Ig? gene enhancers, E3' and Ed, are essential for triggering transcription.

Project description:The mouse Ig? gene locus has three known transcriptional enhancers: an intronic enhancer (Ei), a 3' enhancer (E3'), and a further downstream enhancer (Ed). Previous studies on B lymphocytes derived from mutant embryonic stem cells have shown that deletion of either Ei or E3' significantly reduces Ig? gene rearrangement, whereas the combined deletion of both Ei and E3' eliminates such recombination. Furthermore, deletion of either E3' or Ed significantly reduces rearranged Ig? gene transcription. To determine whether the combined presence of both E3' and Ed are essential for Ig? gene expression, we generated homozygous double knockout (DKO) mice with targeted deletions in both elements. Significantly, homozygous DKO mice were unable to generate ?(+) B cells both in bone marrow and the periphery and exhibited surface expression almost exclusively of Ig?-chains, despite the fact that they possessed potentially functional rearranged Ig? genes. Compared with their single-enhancer-deleted counterparts, Ig? loci in homozygous DKO mice exhibited dramatically reduced germline and rearranged gene transcription, lower levels of gene rearrangement and histone H3 acetylation, and markedly increased DNA methylation. This contributed to a partial developmental block at the pre-B cell stage of development. We conclude that the two downstream enhancers are essential in Ig? gene expression and that Ei in homozygous DKO mice is incapable of triggering Ig? gene transcription. Furthermore, these results reveal unexpected compensatory roles for Ed in E3' knockout mice in triggering germline transcription and V? gene rearrangements to both J? and RS elements.

| S-EPMC3059262 | biostudies-literature

Enhancers predominantly regulate gene expression during differentiation via transcription initiation.

Project description:Gene transcription occurs via a cycle of linked events, including initiation, promoter-proximal pausing, and elongation of RNA polymerase II (Pol II). A key question is how transcriptional enhancers influence these events to control gene expression. Here, we present an approach that evaluates the level and change in promoter-proximal transcription (initiation and pausing) in the context of differential gene expression, genome-wide. This combinatorial approach shows that in primary cells, control of gene expression during differentiation is achieved predominantly via changes in transcription initiation rather than via release of Pol II pausing. Using genetically engineered mouse models, deleted for functionally validated enhancers of the α- and β-globin loci, we confirm that these elements regulate Pol II recruitment and/or initiation to modulate gene expression. Together, our data show that gene expression during differentiation is regulated predominantly at the level of initiation and that enhancers are key effectors of this process.

| S-EPMC7612206 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data