Expression data from E11.5 mouse branchial arch 1 (BA1) - comparison between Ezh2lox/lox and Wnt1Cre Ezh2lox/lox embryos
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE52220 | GEO | 2013/11/09
SECONDARY ACCESSION(S): PRJNA227179
REPOSITORIES: GEO
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Project description:Conditional ablation of Ezh2 in the neural crest lineage results in loss of the neural crest-derived mesenchymal derivatives. In this data sheet we determine gene expression analysis in Ezh2lox/lox and Wnt1Cre Ezh2lox/lox in E11.5 mouse BA1 cells. Conditional ablation of Ezh2 in the neural crest lineage was achieved by crossing Wnt1creEzh2lox/wt mice with Ezh2lox/lox mouse lines. We analyzed a total of 6 samples including 3 biological replicates from Ezh2lox/lox embryos and 3 biological replicates from Wnt1cre Ezh2lox/lox embryos.
2013-11-09 | E-GEOD-52220 | biostudies-arrayexpress
Project description:S23 experiment: We sought to identify the microRNAs (miRNAs) enriched in the neural crest cell (NCC) population from E11.5 mouse embryos. To accomplish this, we utilized a transgenic mouse line harboring Cre-recombinase under the control of the Wnt1 NCC-specific promoter and also carrying the R26R-YFP allele. We sorted YFP+ (NCCs) and YFP- (non-NCCs) from E11.5 Wnt1Cre-R26R mouse embryos via FACS and compared the relative enrichment of miRNAs in the YFP+ population by miRNA microarray. 220 experiment: We sought to identify the microRNAs (miRNAs) enriched in the neural crest cell (NCC) population from E10.5 mouse embryos. To accomplish this, we utilized a transgenic mouse line harboring Cre-recombinase under the control of the Wnt1 NCC-specific promoter and also carrying the R26R-YFP allele. We sorted YFP+ (NCCs) and YFP- (non-NCCs) from E10.5 Wnt1Cre-R26R mouse embryos via FACS and compared the relative enrichment of miRNAs in the YFP+ population by miRNA microarray. 221 experiment: Our research has shown that heterozygous deletion of the miRNA processing enzyme Dicer leads to developmental delay of the thymus in mouse embryos. We sought to identify the microRNAs (miRNAs) affected by the loss of a single copy of Dicer in the neural crest cell (NCC) population from E10.5 mouse embryos. To accomplish this, we utilized a transgenic mouse line harboring a floxed allele of Dicer, Cre-recombinase under the control of the Wnt1 NCC-specific promoter, and also carrying the R26R-YFP allele. We sorted YFP+ (NCCs) cells from E10.5 Dicerfl/+,Wnt1Cre,R26R and Dicer+/+,Wnt1Cre,R26R mouse embryos via FACS and compared the relative expression of miRNAs in the Dicer-heterozygotes compared to Dicer-wildtypes by miRNA microarray. S23 experiment: RNA from YFP+ (NCCs) and YFP- (non-NCCs) cells sorted by FACS from E11.5 Wnt1Cre-R26R mouse embryos was isolated and hybridized to Exiqon miRNA microarrays v10. Cells from five E11.5 embryos were sorted into YFP+ and YFP- populations and pooled. 220 experiment: RNA from YFP+ (NCCs) and YFP- (non-NCCs) cells sorted by FACS from E10.5 Wnt1Cre-R26R mouse embryos was isolated and hybridized to Exiqon miRNA microarrays v10. Cells from ten E10.5 embryos were sorted into YFP+ and YFP- populations and pooled. 221 experiment: RNA from YFP+ (NCCs) cells sorted by FACS from E10.5 Dicerfl/+,Wnt1Cre,R26R and Dicer+/+,Wnt1Cre,R26R mouse embryos was isolated and hybridized to Exiqon miRNA microarrays v10. Cells from ten embryos were sorted into YFP+ populations and pooled for each genotype.
2010-11-10 | E-GEOD-25256 | biostudies-arrayexpress
Project description:S23 experiment: We sought to identify the microRNAs (miRNAs) enriched in the neural crest cell (NCC) population from E11.5 mouse embryos. To accomplish this, we utilized a transgenic mouse line harboring Cre-recombinase under the control of the Wnt1 NCC-specific promoter and also carrying the R26R-YFP allele. We sorted YFP+ (NCCs) and YFP- (non-NCCs) from E11.5 Wnt1Cre-R26R mouse embryos via FACS and compared the relative enrichment of miRNAs in the YFP+ population by miRNA microarray. 220 experiment: We sought to identify the microRNAs (miRNAs) enriched in the neural crest cell (NCC) population from E10.5 mouse embryos. To accomplish this, we utilized a transgenic mouse line harboring Cre-recombinase under the control of the Wnt1 NCC-specific promoter and also carrying the R26R-YFP allele. We sorted YFP+ (NCCs) and YFP- (non-NCCs) from E10.5 Wnt1Cre-R26R mouse embryos via FACS and compared the relative enrichment of miRNAs in the YFP+ population by miRNA microarray. 221 experiment: Our research has shown that heterozygous deletion of the miRNA processing enzyme Dicer leads to developmental delay of the thymus in mouse embryos. We sought to identify the microRNAs (miRNAs) affected by the loss of a single copy of Dicer in the neural crest cell (NCC) population from E10.5 mouse embryos. To accomplish this, we utilized a transgenic mouse line harboring a floxed allele of Dicer, Cre-recombinase under the control of the Wnt1 NCC-specific promoter, and also carrying the R26R-YFP allele. We sorted YFP+ (NCCs) cells from E10.5 Dicerfl/+,Wnt1Cre,R26R and Dicer+/+,Wnt1Cre,R26R mouse embryos via FACS and compared the relative expression of miRNAs in the Dicer-heterozygotes compared to Dicer-wildtypes by miRNA microarray.
2010-11-10 | GSE25256 | GEO
Project description:Cranial neural crest cells (NCC) give rise to the majority of the cartilage, bone, connective tissue, and sensory ganglia in the head, and also participate in the remodeling of the cardiac outflow tract and pharyngeal arch arteries during cardiovascular development. Our preliminary results show that targeted deletion of focal adhesion kinase (FAK) in murine NCC results in cardiovascular and craniofacial alterations, resembling human congenital heart diseases The objective of this project is to elucidate the underlying mechanisms by which FAK mediates NCC function during development. Compare gene expression in cranial neural crest cells of E11.5 wild type and FAK mutants. FAK is a tyrosine kinase that transduces integrin and growth factor signaling pathways. Abnormal growth factor signaling leads to cardiovascular malformations caused by deficient cardiac NCC function. However, a direct role for FAK in NCC morphogenesis has not been demonstrated. We will test the hypothesis that FAK is a downstream target of essential growth factor signaling in cranial neural crest cells during development. 1) Generate E11.5 mouse embryos that are either control (FAK+/flox) or NCC specific FAK knockout (Wnt1Cre;FAKflox/flox). 2) Determine genotype by PCR. 3) Dissect head and torax from the different genotypes. 4) Obtain NCC from dissected tissue by magnetic cell sorting using p75 antibody. 5) Prepare total RNA from speciments. We will pool the NCC from 3 different embryos of the same genotype, and send total RNA to TGEN for probe preparation, hybridization and array result analysis.
2008-06-11 | E-GEOD-11149 | biostudies-arrayexpress
Project description:Cranial neural crest cells (NCC) give rise to the majority of the cartilage, bone, connective tissue, and sensory ganglia in the head, and also participate in the remodeling of the cardiac outflow tract and pharyngeal arch arteries during cardiovascular development. Our preliminary results show that targeted deletion of focal adhesion kinase (FAK) in murine NCC results in cardiovascular and craniofacial alterations, resembling human congenital heart diseases The objective of this project is to elucidate the underlying mechanisms by which FAK mediates NCC function during development. Compare gene expression in cranial neural crest cells of E11.5 wild type and FAK mutants. FAK is a tyrosine kinase that transduces integrin and growth factor signaling pathways. Abnormal growth factor signaling leads to cardiovascular malformations caused by deficient cardiac NCC function. However, a direct role for FAK in NCC morphogenesis has not been demonstrated. We will test the hypothesis that FAK is a downstream target of essential growth factor signaling in cranial neural crest cells during development. 1) Generate E11.5 mouse embryos that are either control (FAK+/flox) or NCC specific FAK knockout (Wnt1Cre;FAKflox/flox). 2) Determine genotype by PCR. 3) Dissect head and torax from the different genotypes. 4) Obtain NCC from dissected tissue by magnetic cell sorting using p75 antibody. 5) Prepare total RNA from speciments. We will pool the NCC from 3 different embryos of the same genotype, and send total RNA to TGEN for probe preparation, hybridization and array result analysis. Keywords: other
2008-05-06 | GSE11149 | GEO
Project description:We conditionally knocked out both Yap and Taz in cranial neural crest (CNC) using the Wnt1Cre driver and sequenced mRNA from embryonic day 10.5 mandibles. Examination of mRNA level in E10.5 mandibular tissues from control and Wnt1Cre Taz and Yap dKO mutant.
2016-03-01 | E-GEOD-69311 | biostudies-arrayexpress
Project description:Purpose: Determine how blocking retinoic acid receptor (RAR) signaling within enteric neural crest-derived cells (ENCDC) from E11.5 stomach or E13.5 colon alters mRNA abundance. These ENCDC become the enteric nervous system. Methods: Enteric nervous system precursors were isolated from mouse E11.5 stomach or E13.5 colon using fluorescence activated cell sorting to purify TdTomato or EYFP expressing cells respectively from fetal bowel. The RarαDN allele encodes a potent RAR dominant negative protein that is expressed after CRE-mediated DNA recombination. Tamoxifen-activated CRE-ERT2 was expressed from the Ret locus for E13.5 colon studies and mice were tamoxifen treated at E10.5 prior to cell sorting. The Wnt1Cre allele was employed for E11.5 stomach studies. RNA-SEQ was performed in quadruplicate using Illumina HiSeq 4000. Sequence reads that passed quality filters were aligned to remove repeat sequences and ribosomal RNA reads and then processed using RNA-Seq unified mapper (RUM) package. RUM files were visualized in the TessLA browser for subsequent analyses. Results: Transcriptional profiling shows RarαDN differentially impacts gene expression in E11.5 stomach and E13.5 colon enteric neural crest-derived cells (ENCDC) that become the enteric nervous system. Conclusions: Blocking of RAR signaling in ENCDC causes dramatic changes in gene expression during early development in a stage-specific manner.
2021-02-04 | GSE165344 | GEO
Project description:We conditionally knocked out both Yap and Taz in cranial neural crest (CNC) using the Wnt1Cre driver and sequenced mRNA from embryonic day 10.5 mandibles.
2016-03-01 | GSE69311 | GEO
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.
2014-06-18 | GSE52357 | GEO
Project description:Expression data from E11.5 mouse branchial arch 1 (BA1) - comparison between Ezh2lox/lox and Wnt1Cre Ezh2lox/lox embryos
| PRJNA227179 | ENA