Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single cell RNA-seq analysis of CNCCs at embryonic E9.5

ABSTRACT: Cardiac NCC were extracted by dissecting out Prdm6f/f; Wnt1-Cre2; ZsGreen1 embryos and their wildtype littermates (Prdm6+/+; Wnt1-Cre2; ZsGreen1) from mid otic placode to the posterior edge of the 4th somite. The ScRNA-seq was carried out using the 10X Genomics Chromium system. There was an average of 2,742 and 3,102 counts per cell or an average of 1,294 and 1,432 unique genes detected in respectively WT and KO conditions. In our models we show that the absence of Prdm6 tips the balance in favor of Wnt1 by reducing Bmp4 and increasing Wnt1 transcripts in several clusters, leading to impaired CNCC migration.

ORGANISM(S): Mus musculus

PROVIDER: GSE195589 | GEO | 2022/01/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Chick Otic Placode Induction Arrays

Project description:The inner ear develops from a patch of thickened cranial ectoderm adjacent to the hindbrain called the otic placode. Studies in a number of vertebrate species suggest that the initial steps in induction of the otic placode are regulated by members of the Fibroblast Growth Factor (FGF) family, and that inhibition of FGF signaling can prevent otic placode formation. To better understand the genetic pathways activated by FGF signaling during otic placode induction, we performed microarray experiments to estimate the proportion of chicken otic placode genes that can be up-regulated by the FGF pathway in a simple culture model of otic placode induction. Surprisingly, we find that FGF is only sufficient to induce about 15% of chick otic placode-specific genes in our experimental system. However, pharmacological blockade of the FGF pathway in cultured chick embryos showed that although FGF signaling was not sufficient to induce the majority of otic placode-specific genes, it was still necessary for their expression in vivo. These inhibitor experiments further suggest that the early steps in otic placode induction regulated by FGF signaling occur through the MAP kinase pathway. Although our work suggests that FGF signaling is necessary for otic placode induction, it demonstrates that other unidentified signaling pathways are required to co-operate with FGF signaling to induce the full otic placode program. 8 samples were analyzed. These contain two replicates of each of the following four catergories: Otic ectoderm, Non-Otic (lateral) ectoderm, Trigeminal Ectoderm cultured - FGF, Trigeminal Ectoderm cultured + FGF

2012-12-12 | E-GEOD-42845 | biostudies-arrayexpress

Chick Otic Placode Induction Arrays

2012-12-12 | GSE42845 | GEO

Identification of differentially expressed genes in early inner ear development

Project description:The first morphological evidence of the developing ear is a thickened disk of ectoderm known as the otic placode. However, signals for otogenesis are present even before the otic placode is physically apparent. Several inductive signals have been identified through candidate gene approaches, but there are still many gaps in the signaling cascade of otogenesis. Presently the candidate gene approach has largely exhausted known candidates. This project compares the pre-otic domain with a control region that is competent, but not specified to form otic placode. The purpose of this work is to identify genes that are differentially expressed in the pre-otic domain in order to generate a list of novel candidate genes for otic placode induction.

2010-06-21 | GSE16918 | GEO

Heterogeneous Cardiac- and Neural Crest-Derived Aortic Smooth Muscle Cells have Similar Transcriptional Changes after TGFβ Signaling Disruption [scRNA-seq-of-Wnt1-Cre2-mTmG]

Project description:We report single-cell RNA-seq data of Wnt1-Cre2 lineage marked, integrin alpha 8 labeled smooth muscle cells (SMCs) from murine aortas at 12 weeks of age

2025-02-27 | GSE253930 | GEO

Gallus gallus

Project description:Chick Otic Placode Induction Arrays

| PRJNA183635 | ENA

Murine Fgf3-/-;Fgf10-/- vs. Fgf3+/-;Fgf10+/- otic placode profiling

2010-03-01 | GSE18702 | GEO

Murine Fgf3-/-;Fgf10-/- vs. Fgf3+/-;Fgf10+/- otic placode profiling

Project description:Transcriptional profiling of mouse 4-8 somite microdissected otic placodes from Fgf3/Fgf10 double heterozygotes (controls) compared to Fgf3/Fgf10 double null mutants. The purpose was to determine the effectors that are induced (or repressed) by Fgf3 and Fgf10 in the course of otic placode induction. Two condition experiment, double heterozygote vs. double null placodes. Biological replicas: 3 Fgf3+/-;Fgf10+/- and 3 Fgf3-/-;Fgf10-/- pools of ten placodes each.

2010-03-07 | E-GEOD-18702 | biostudies-arrayexpress

Gene expression profiling of the tongue bud from Alk5 mutant mouse models

Project description:The overall goal of this project is to investigate the role of TGF-beta signaling in tissue-tissue interactions between myogenic precursors of craniofacial muscles and cranial neural crest cells (CNCCs). Here, we conducted gene expression profiling of the tongue bud from mice at embryonic day E13.5 with a CNCC-specific conditional inactivation of the TGF-beta receptor type 1 gene Alk5. These mice provide a model of microglossia as well as disrupted extraocular and masticatory muscle development, which are congenital birth defects commonly observed in several syndromic conditions. To investigate the adverse effects of dysfunctional TGF-beta signaling on tissue-tissue interactions between CNCCs and myogenic precursors of craniofacial muscles, we analyzed tongue bud tissue of mice with a CNCC-specific conditional inactivation of Alk5 (Wnt1-Cre; Alk5 fl/fl). We performed microarray analyses of the tongue bud of Alk5 fl/fl control mice and Wnt1-Cre; Alk5 fl/fl mutant mice, collected at embryonic day E13.5 (n=4 per group).

2014-06-18 | E-GEOD-52358 | biostudies-arrayexpress

Gene expression profiling of the mandibular arch from Alk5 mutant mouse models

Project description:The overall goal of this project is to investigate the role of TGF-beta signaling in tissue-tissue interactions between myogenic precursors of craniofacial muscles and cranial neural crest cells (CNCCs). Here, we conducted gene expression profiling of the mandibular arch from mice at embryonic day E11.5 with a CNCC-specific conditional inactivation of the TGF-beta receptor type 1 gene Alk5. These mice provide a model of microglossia as well as disrupted extraocular and masticatory muscle development, which are congenital birth defects commonly observed in several syndromic conditions. To investigate the adverse effects of dysfunctional TGF-beta signaling on tissue-tissue interactions between CNCCs and myogenic precursors of craniofacial muscles, we analyzed mandibular arch tissue of mice with a CNCC-specific conditional inactivation of Alk5 (Wnt1-Cre; Alk5 fl/fl). We performed microarray analyses of the mandibular arch of Alk5 fl/fl control mice and Wnt1-Cre; Alk5 fl/fl mutant mice, collected at embryonic day E11.5 (n=4 per group).

2014-06-18 | E-GEOD-52357 | biostudies-arrayexpress

Critical role of FGF, RA, and WNT signaling for otic lineage specification from human PSCs in a 2D/3D-combined differentiation system

Project description:The otic placode, from which the inner ear develops, initially forms as a thickened ectodermal patch adjacent to the dorsolateral hindbrain. Induction of otic placodal cells from human pluripotent stem cells (hPSCs) provides a robust approach to investigation of otic development. However, attempts to recapitulate otic lineage specification from hPSCs by stepwise differentiation methods have had limited success. One possible reason is that the role of signaling pathways in otic cell differentiation is not fully understood. Here, we developed a novel differentiation system involving use of suspension culture (3D floating culture) in combination with signaling factors for generating otic placodal cells via stepwise differentiation of hPSCs. We demonstrate that hPSC-derived pre-placodal cells acquired the potential to differentiate into posterior placodal cells after fibroblast growth factor 2 (FGF2) and retinoic acid (RA) treatment. Subsequent activation of WNT signaling following posterior placode specification induced differentiation of SIX1+/PAX8+/SOX2+ otic placodal cells. qPCR analysis showed that WNT activation increased expression of otocyst markers, including PAX8, PAX2, DLX5 and FBXO2. Moreover, induced otic cells exhibited similar gene expression patterns to the ventral and medial portions of the otocyst that give rise to the sensory epithelium of the inner ear. Collectively, our results indicate a critical role for FGF2, RA, and WNT signaling for the in vitro differentiation of the otic cell lineage from hPSCs. Our new culture system paves the way for improved modeling of early human inner ear development and will be of value to studies on the further differentiation of sensory epithelial cells.

2022-02-01 | GSE175998 | GEO

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