Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-cell transcriptomics uncovers a non-autonomous Tbx1-dependent genetic program controlling cardiac neural crest cell development

ABSTRACT: Single-cell transcriptomics uncovers a non-autonomous Tbx1-dependent genetic program controlling cardiac neural crest cell development

PROVIDER: PRJNA866098 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR20825400_1.fastq.gz	Fastqsanger.gz
	SRR20825400_2.fastq.gz	Fastqsanger.gz
	SRR20825401_1.fastq.gz	Fastqsanger.gz
	SRR20825401_2.fastq.gz	Fastqsanger.gz
	SRR20825402_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 14

Similar Datasets

Single-cell transcriptomics uncovers a non-autonomous Tbx1-dependent genetic program controlling cardiac neural crest cell development

Project description:Disruption of cardiac neural crest cells (CNCCs) results in congenital heart disease, yet we do not understand the cell fate dynamics as these cells differentiate to vascular smooth muscle cells. Here we performed single-cell RNA-sequencing of NCCs from the pharyngeal apparatus with the heart in control mouse embryos and when Tbx1, the gene for 22q11.2 deletion syndrome, is inactivated. We uncover three dynamic transitions of pharyngeal NCCs expressing Tbx2 and Tbx3 through differentiated CNCCs expressing cardiac transcription factors with smooth muscle genes. These transitions are altered non-autonomously by loss of Tbx1. Further, inactivation of Tbx2 and Tbx3 in early CNCCs results in aortic arch branching defects due to failed smooth muscle differentiation. Loss of Tbx1 interrupts mesoderm to CNCC cell-cell communication with upregulation and premature activation of BMP signaling and reduced MAPK signaling, as well as alteration of other signaling, and failed dynamic transitions of CNCCs leading to disruption of aortic arch artery formation and cardiac outflow tract septation.

2023-02-13 | GSE210521 | GEO

Single-cell transcriptomics uncovers a non-autonomous Tbx1-dependent genetic program controlling cardiac neural crest cell development.

| S-EPMC10027855 | biostudies-literature

scATAC-seq over multiple time points of heart development in WT C57Bl6/J embryos and in Tbx1 mutant mice (Tbx1 KO)

Project description:We performed scATAC-seq over multiple time points of heart development in WT C57Bl6/J embryos and in Tbx1 mutant mice (Tbx1 KO). We dissected primarily the cardiac region but also the regions dorsal to the heart and the pharyngeal arches to capture the progenitor cells that migrate into the heart and the neural crest cells. For time points E10.5 and E11.5, we primarily dissected the regions behind the heart and included less of the overall cardiac region. We included pharyngeal arches for all time points and, at E11.5, we excluded the first arch. For Tbx1 null embryos, we also generated scRNA-seq data for WT and mutant embryos from the same pool of dissociated cells used for scATAC-seq.

2022-07-27 | GSE198561 | GEO

scRNA-seq over multiple time points of heart development in WT C57Bl6/J embryos and in Tbx1 mutant mice (Tbx1 KO)

Project description:We performed scRNA-seq over multiple time points of heart development in WT C57Bl6/J embryos and in Tbx1 mutant mice (Tbx1 KO). We dissected primarily the cardiac region but also the regions dorsal to the heart and the pharyngeal arches to capture the progenitor cells that migrate into the heart and the neural crest cells. For time points E10.5 and E11.5, we primarily dissected the regions behind the heart and included less of the overall cardiac region. We included pharyngeal arches for all time points and, at E11.5, we excluded the first arch. For Tbx1 null embryos, we also generated scRNA-seq data for WT and mutant embryos from the same pool of dissociated cells used for scATAC-seq.

2022-07-27 | GSE198562 | GEO

Transcription profiling of Tbx1 function in adult myocardial infarction hearts [bulk RNA-seq]

Project description:Post-myocardial infarction (Post-MI) heart failure is an unanswered clinical challenge. Current immunological intervention trials to reduce MI damage are unsatisfactory. Tbx1, the major 22q11.2 deletion syndrome (22q11.2DS) disease gene, reactivated in cardiac lymphatic endothelial cells (LECs) to promote post-MI repair. Endothelial deletion of Tbx1 deteriorated post-MI cardiac function. To identify the initial endothelial-derived gene expression changes that are responsible for lymphangiogenesis and cell non-autonomous functions towards immune cells after MI, we enriched CD31+ endothelial cells from 5 dpMI Ctrl and Tbx1cko hearts and performed RNA-seq. In conclusion, our findings revealed that Tbx1 can promote lymphangiogenesis and alleviate excessive cardiac inflammation in post MI hearts.

2023-08-28 | GSE137063 | GEO

Gene profiling on mandibular arches (MdPA1) from Tbx1+/+ and Tbx1-/- mouse embryos

2014-05-21 | GSE30980 | GEO

Gene profiling on mandibular arches (MdPA1) from Tbx1+/+ and Tbx1-/- mouse embryos E9.5

Project description:Velo-cardio-facial syndrome/DiGeorge syndrome/22q11.2 deletion syndrome (22q11DS) patients have a submucous cleft palate, velo-pharyngeal insufficiency associated with hypernasal speech, facial muscle hypotonia and feeding difficulties. Inactivation of both alleles of mouse Tbx1, encoding a T-box transcription factor, deleted on 22q11.2, results in a cleft palate and a reduction or loss of branchiomeric muscles. To identify genes downstream of Tbx1 for myogenesis, gene profiling was performed on mandibular arches (MdPA1) from Tbx1+/+ and Tbx1-/- mouse embryos. To obtain enough RNA for microarray hybridization experiments, dissected mandibular arches from three Tbx1+/+ and three Tbx1-/- E9.5 embryos were pooled according to genotype, with three microarrays performed in total per genotype. Affymetrix Mouse Gene ST 1.0 arrays (Affymetrix) were used. Hybridization, washing, staining and scanning were performed in the Genomics Core at Einstein (http://www.einstein.yu.edu/genetics/CoreFacilities.aspx?id=23934) according to the Affymetrix manual.

2014-05-21 | E-GEOD-35013 | biostudies-arrayexpress

Gene profiling on mandibular arches (MdPA1) from Tbx1+/+ and Tbx1-/- mouse embryos E9.5

2014-05-21 | GSE35013 | GEO

Transcription profiling of mouse embryonic cells (E9.5) with homozygous knockout of Tbx1 compared to heterozygous Tbx1 knockout

Project description:22q11 deletion syndrome (22q11DS) is mainly characterised by cardiovascular, craniofacial, thymic and parathyroid abnormalities. Haploinsufficiency of the transcription factor, TBX1 is considered to be a major underlying cause of these defects. Mice in which Tbx1 has been mutated phenocopy 22q11DS. In order to elucidate the transcriptional pathways regulated by Tbx1, the gene expression profile of Tbx1-lacZ positive cells isolated from E9.5 Df1/Tbx1lacZ embryos (Tbx1-null) were compared to cells isolated from Tbx1+/lacZ (Tbx1-heterozygous) embryos. This analysis has led to a better understanding of the pathways important in pharyngeal and heart development. Experiment design: 3 pools of cells (biological replicates) isolated from Df1/Tbx1lacZ embryos and Tbx1+/lacZ embryos were used for hybridisation onto 6 MOE430 v2 oligonucleotide array chips (Affymetrix), making 12 microarrays in total. Each pool of cells was isolated from at least 8 embryos.

2009-05-30 | E-MEXP-2096 | biostudies-arrayexpress

Single cell RNAseq profiling of Tbx1 function in adult post myocardial infarction hearts [scRNA-seq]

Project description:Post-myocardial infarction (Post-MI) heart failure is an unanswered clinical challenge. Current immunological intervention trials to reduce MI damage are unsatisfactory. Thus a thorough understanding of post-MI immune response is imperative. Tbx1, the major 22q11.2 deletion syndrome (22q11.2DS) disease gene, reactivated in cardiac lymphatic endothelial cells (LECs) to promote post-MI repair. Endothelial deletion of Tbx1 deteriorated post-MI cardiac function through a dual approach, impaired lymphangiogenesis and weakened immunosuppression. To characterize cell autonous function of Tbx1 in endothelial population and cell non-autonous effect in immune cells, we set to performed scRNA-seq on Ctrl (Tbx1flox/flox) and Tbx1cko (Fabp4-Cre;Tbx1flox/flox) hearts. The dataset is comprised of total 55,106 single cells transcriptomes. We identified eight principal non-myocyte types with their known markers, including CD31-expressing vascular endothelial cell (VEC), LEC, pericyte, as well as CD45-expressing monocyte/macrophage, dendritic cell (DC), neutrophil, T/innate lymphoid cell (ILC), and B cell. Interestingly, we found that the relative percentage of monocyte/macrophage population, which is most abundant among all immune cells, was significantly decreased in Tbx1cko hearts, whereas T/ILC population was increased. Taken together, single cell transcriptomic analyses suggest a potential cell non-autonomous effect that Tbx1 deficiency in endothelium may cause imbalance in immune response.

2023-08-28 | GSE136762 | 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