Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Programmed genomic instability regulates neural transdifferentiation of human brain microvascular pericytes [ATAC-Seq]

ABSTRACT: The observation that human microvascular pericytes transdifferentiate into neurons provided an opportunity to explore the endogenous molecular basis for lineage reprogramming. Here, we show that abrupt destabilization of the higher-order chromatin topology that chaperones lineage memory of pericytes is driven by transient global transcriptional arrest. This leads within minutes to localized decompression of the repressed competing higher-order chromatin topology and expression of pro-neural genes. Transition to neural lineage is completed by probabilistic induction of R-loops in key myogenic loci upon re-initiation of RNA polymerase activity, leading to depletion of the myogenic transcriptome and emergence of the neurogenic transcriptome.

ORGANISM(S): Homo sapiens

PROVIDER: GSE187016 | GEO | 2021/11/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Shared Molecules

Only show the datasets with similarity scores above: 0.5

Threshold

0.5

Similar Datasets

Programmed genomic instability regulates neural transdifferentiation of human brain microvascular pericytes [RNA-Seq]

Project description:The observation that human microvascular pericytes transdifferentiate into neurons provided an opportunity to explore the endogenous molecular basis for lineage reprogramming. Here, we show that abrupt destabilization of the higher-order chromatin topology that chaperones lineage memory of pericytes is driven by transient global transcriptional arrest. This leads within minutes to localized decompression of the repressed competing higher-order chromatin topology and expression of pro-neural genes. Transition to neural lineage is completed by probabilistic induction of R-loops in key myogenic loci upon re-initiation of RNA polymerase activity, leading to depletion of the myogenic transcriptome and emergence of the neurogenic transcriptome.

2021-11-04 | GSE187019 | GEO

Programmed genomic instability regulates neural transdifferentiation of human brain microvascular pericytes [DRIP-Seq]

2021-11-04 | GSE187018 | GEO

Programmed genomic instability regulates neural transdifferentiation of human brain microvascular pericytes [ChIP-Seq]

2021-11-04 | GSE187017 | GEO

NG2+ and Tbx18+ pericyte subtypes exhibit distinct reprogramming potency following ischemic stroke

Project description:Increasing evidence shows that brain pericytes can acquire multipotency to produce multi-lineage cells following injury. However, pericytes are a heterogenous population and it remains unknown whether there are different potencies from different subsets of pericytes in response to injury. Here, using single-cell RNA-sequencing (scRNA-seq) and immunohistochemistry analysis following ischemic stroke, we showed that NG2+ pericyte subset expressed very strong neural reprogramming potential to produce newborn neurons, while Tbx18+ pericytes displayed strong multipotency to produce endothelial cells, fibroblasts, and microglia but with minimal neural reprogramming potency. In addition, we mimicked ischemic stroke in vitro and developed an NG2+ pericyte neural reprogramming culture model. Here we discovered that AMP-dependent kinase (AMPK) modulators facilitated pericyte to neuron conversion by modulating Ser436 phosphorylation status of CREB-binding protein (Cbp), a histone acetyltransferase, which coordinated an acetylation shift between the non-histone substrate (Sox2) and the histone substrate (H2B) and modulated Sox2 nuclear-cytoplasmic trafficking during reprogramming/differentiation process. Finally, we identified that sequential treatment of compound C (CpdC) and metformin, AMPK inhibitor and activator respectively through reprogramming/differentiation process, robustly facilitated the conversion of human pericyte into functional neurons via transient pericyte-derived neural stem cell population.

2024-10-01 | GSE250597 | GEO

Incomplete MyoD-induced transdifferentiation is mediated by chromatin remodeling deficiencies [RNA-Seq]

Project description:MyoD is known to transdifferentiate fibroblasts into muscle-like cells. Despite phenotypic resemblance and expression of myogenic marker genes in transdifferentiated cells, our global gene expression data suggests that ~100 genes, many involved in muscle development and function, remain non-reprogrammed. To understand this incomplete reprogramming, we characterized genome-wide chromatin accessibility and MyoD binding in human primary myoblasts and in MyoD-induced skin fibroblast cells. Our analyses revealed thousands of sites with incomplete chromatin reprogramming.Combined analyses of gene expression and epigenetic profiles revealed that many myogenic genes not upregulated during the transdifferentiation process have undergone MyoD-dependent chromatin remodeling, but to a significantly lower extent than reprogrammed genes. Our findings suggest that incomplete MyoD-induced transdifferentiation is due to chromatin-remodeling deficiencies, and that additional factors are required to transdifferentiate cells into a state more similar to myoblasts.

2017-01-07 | GSE93263 | GEO

Incomplete MyoD-induced transdifferentiation is mediated by chromatin remodeling deficiencies [ChIP-Seq]

2017-01-07 | GSE93258 | GEO

Incomplete MyoD-induced transdifferentiation is mediated by chromatin remodeling deficiencies [Dnase-Seq]

2017-01-07 | GSE93257 | GEO

Chemical reprogramming of melanocytes to skeletal muscle cells

Project description:We identify a combination of small molecules to be able to transdifferentiate dermal cells to muscle cells. To characterize the cellular diversity of the neonatal dermal we performed scRNA-seq on mononuclear cell suspensions obtained from the neonatal dermal. Following normalization and quality control of scRNA-seq data, we captured 40537 cells with an average of 5755 genes expressed per cell. We charted the entire course of skin-to-muscle chemical reprogramming by single cell RNA-sequencing to determine the source cells in CD73- cells from skin with the potential to be transdifferentiated to muscle cells .We found that melanocytes could be chemically reprogrammed to myogenic lineage cells.

2023-02-03 | GSE213195 | GEO

Dynamics of embryonic stem cell differentiation inferred from single-cell transcriptomics show a series of transitions through discrete cell states

Project description:Using a statistical framework to analyze single-cell transcriptomics data, we infer the gene expression dynamics of early mouse embryonic stem (mES) cell differentiation, uncovering discrete transitions across nine cell states. We validate the predicted transitions across discrete states using flow cytometry. Moreover, using live-cell microscopy, we show that individual cells undergo abrupt transitions from a naïve to primed pluripotent state. Using the inferred discrete cell states to build a probabilistic model for the underlying gene regulatory network, we further predict and experimentally verify that these states have unique response to perturbations, thus defining them functionally.

2017-10-17 | GSE105054 | GEO

Sebastes melanops array 5K v1

Project description:We used a reference design with a dye swap. We used 6 experimental probes grouped by treatment and sample day. "Treatment" fish consisted of rockfish exposed to forced decompression resulting in barotrauma, followed by subsequent recompression to their original depth. Control fish did not experience forced decompression. Fish were sampled at day 3, day 15 and day 31 post-decompression.

2012-01-02 | E-MEXP-3087 | biostudies-arrayexpress

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