Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Profile of Bmpr1a-/- embryonic stem cells in ESC media and N2B27

ABSTRACT: A fundamental question in developmental biology is whether there are mechanisms to detect stem cells with mutations that although do not adversely affect their viability, would compromise their ability to contribute to further development. Here we show that cell competition is a novel mechanism regulating the fitness of embryonic stem cells (ESCs). We find that ESCs displaying defective BMP signalling, defective autophagy or are tetraploid are eliminated at the onset of differentiation by wild-type cells. This elimination occurs in an apoptotic dependent manner and is mediated by secreted factors. Furthermore, during this process we find that establishment of differential cMyc levels is critical and that cMyc over-expression is sufficient to induce competitive behaviour in ESCs. Cell competition is therefore a process that allows recognition and elimination of defective cells during the early stages of development and is likely to play important roles in tissue homeostasis and stem cell maintenance. We used microarrays to compare the gene expression profiles of Bmpr1a-/- and control embryonic stem cells (ESCs) in the ESC state and after differentiation in N2B27

ORGANISM(S): Mus musculus

PROVIDER: GSE48092 | GEO | 2013/06/20

SECONDARY ACCESSION(S): PRJNA208900

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Profile of Bmpr1a-/- embryonic stem cells in ESC media and N2B27

Project description:A fundamental question in developmental biology is whether there are mechanisms to detect stem cells with mutations that although do not adversely affect their viability, would compromise their ability to contribute to further development. Here we show that cell competition is a novel mechanism regulating the fitness of embryonic stem cells (ESCs). We find that ESCs displaying defective BMP signalling, defective autophagy or are tetraploid are eliminated at the onset of differentiation by wild-type cells. This elimination occurs in an apoptotic dependent manner and is mediated by secreted factors. Furthermore, during this process we find that establishment of differential cMyc levels is critical and that cMyc over-expression is sufficient to induce competitive behaviour in ESCs. Cell competition is therefore a process that allows recognition and elimination of defective cells during the early stages of development and is likely to play important roles in tissue homeostasis and stem cell maintenance. We used microarrays to compare the gene expression profiles of Bmpr1a-/- and control embryonic stem cells (ESCs) in the ESC state and after differentiation in N2B27 Microarray profiles of control and Bmpr1a-/- mouse embryonic stem cells in embryonic stem cell culture media and in N2B27

2013-06-20 | E-GEOD-48092 | biostudies-arrayexpress

Microarray analysis of gene expression during ESC cell competition

Project description:A fundamental question in developmental biology is whether there are mechanisms to detect stem cells with mutations that, although not adversely affecting viability, would compromise their ability to contribute to further development. Here, we show that cell competition is a mechanism regulating the fitness of embryonic stem cells (ESCs). We find that ESCs displaying defective bone morphogenetic protein signaling or defective autophagy or that are tetraploid are eliminated at the onset of differentiation by wild-type cells. This elimination occurs in an apoptosis-dependent manner and is mediated by secreted factors. Furthermore, during this process, we find that establishment of differential c-Myc levels is critical and that c-Myc overexpression is sufficient to induce competitive behavior in ESCs. Cell competition is, therefore, a process that allows recognition and elimination of defective cells during the early stages of development and is likely to play important roles in tissue homeostasis and stem cell maintenance.

2018-01-24 | GSE109494 | GEO

Hormone-responsive Bmpr1a maintains myoepithelial integrity during pregnancy

Project description:Myoepithelial and luminal cells synergistically expand in the mammary gland during pregnancy, and this process is precisely governed by hormone-related signaling pathways. The BMP signaling pathway is now known to play crucial roles in all organ systems. However, the functions of BMP signaling in the mammary gland remain unclear. Here, we found that Bmpr1a is upregulated by hormone-induced Sp1 at pregnancy. Using a doxycycline (Dox)-inducible Bmpr1a conditional knockout mouse model, we demonstrated that loss of Bmpr1a results in compromised myoepithelial integrity, reduced mammary stem cells and precocious alveolar differentiation during pregnancy. Mechanistically, Bmpr1a regulates the expression of p63 and Slug, two key regulators of myoepithelial maintenance, through pSmad1/5-Smad4 complexes, and consequently activate P-cadherin during pregnancy. Collectively, these findings identify a novel role of BMP signaling in maintaining the identity of myoepithelial cells and suppressing precocious alveolar formation.

2021-03-05 | GSE164550 | GEO

Neural induction (N2B27 monolayer cluture)

Project description:Neural induction of ES by N2B27 monolayer culture Keywords: development or differentiation design,time series design

2006-01-23 | GSE4076 | GEO

Gene expression microarray for mouse ES cells vs. mouse ES cells treated with 48 hr N2B27

Project description:Core circuits of transcription factors stabilize stem and progenitor cells by suppressing genes required for differentiation. We do not know how such core circuits are reorganized during cell fate transitions to allow differentiation and lineage choice to proceed. Here, we asked how the pluripotency circuit, a core transcriptional circuit that maintains mouse embryonic stem (ES) cells in a pluripotent state, is dismantled as ES cells differentiate and choose between the neural ectodermal and mesendodermal progenitor cell fates. When ES cells are recultured from pluripotency maintaining conditions to the basal media N2B27, the expression of the pluripotency circuit genes begins to change. At 48 hours post N2B27 addition, the ES cells are competent to respond to differentiation signals. Here, our microarray analysis compares the gene expression profile of ES cells vs. the gene expression profile of cells that have been treated with N2B27 for 48 hours, reaching the competent state.

2011-05-03 | GSE29005 | GEO

Neural induction (N2B27 monolayer cluture)

Project description:Neural induction of ES by N2B27 monolayer culture Neural induction of ES by N2B27 monolayer culture

2006-01-22 | E-GEOD-4076 | biostudies-arrayexpress

Mus musculus

Project description:Profile of Bmpr1a-/- embryonic stem cells in ESC media and N2B27

| PRJNA208900 | ENA

ES, EC, NS, TS, Placenta and Neural induction (N2B27) comaprison

Project description:Comparison among ES, EC, TS, NS, differentiated neural cells derived from NS and placenta in addition to ES-N2B27 neural induction. Keywords: cell type comparison design,development or differentiation design,time series design

2006-01-23 | GSE4077 | GEO

Gene expression microarray for mouse ES cells vs. mouse ES cells treated with 48 hr N2B27

2011-05-03 | E-GEOD-29005 | biostudies-arrayexpress

Next-generation RNA Sequencing and Transcriptome Comparison of Mouse Wild Type and Mesenchymal Bmpr1a conditional knockout lungs of E15.5

Project description:Lung mesenchymal knockout of Bmpr1a will lead to lung malformation, including impaired lung branching and cystic lesion. In order to understand the underlying mechanisms, total RNA of wild type and mesenchymal Bmpr1a knockout lungs were isolated and sequenced using the next-generation RNA sequencing technique.

2024-04-01 | GSE97946 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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