TBX5 KO HiChIP
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA920798 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23009833_1.fastq.gz | Fastqsanger.gz | |||
| SRR23009833_2.fastq.gz | Fastqsanger.gz | |||
| SRR23009834_1.fastq.gz | Fastqsanger.gz | |||
| SRR23009834_2.fastq.gz | Fastqsanger.gz | |||
| SRR23009835_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
Similar Datasets
Project description:Understanding how the atrial and ventricular chambers of the heart maintain their distinct identity is a prerequisite for treating chamber-specific diseases. Here, we selectively inactivated the transcription factor Tbx5 in the atrial working myocardium of the neonatal mouse heart to show that it is required to maintain atrial identity. Atrial Tbx5 inactivation downregulated highly chamber specific genes such as Myl7 and Nppa, and increased expression of ventricular identity genes including Myl2. Using combined single nucleus transcriptome and open chromatin profiling, we assessed genomic accessibility changes underlying the altered atrial identity expression program, identifying 1846 genomic loci with greater accessibility in control atrial cardiomyocytes compared to KO aCMs. 69% of the control-enriched ATAC regions were bound by TBX5, demonstrating a role for TBX5 in maintaining genomic accessibility. These regions were associated with genes that had higher expression in control aCMs compared to KO aCMs, suggesting they act as TBX5-dependent enhancers. To confirm this hypothesis we analyzed chromatin looping of enhancers marked by H3K27Ac using HiChIP and found 510 chromatin loops that were sensitive to TBX5 dosage. Of the loops enriched in control aCMs, 73.7% contained anchors in control-enriched ATAC regions. Conversely, Tbx5 overexpression in the ventricular myocardium drove atrial gene expression. Together, these data demonstrate a role for TBX5 in maintaining the atrial gene expression program by binding to atrial enhancers to preserve tissue-specific chromatin architecture. We highlight this phenomenon at major atrial identity genes including Nppa, Bmp10 and Myl7. HiChIP for H3K27Ac from atria of TBX5KO and control animals
2023-08-11 | GSE222370 | GEO
Project description:Understanding how the atrial and ventricular chambers of the heart maintain their distinct identity is a prerequisite for treating chamber-specific diseases. Here, we selectively inactivated the transcription factor Tbx5 in the atrial working myocardium of the neonatal mouse heart to show that it is required to maintain atrial identity. Atrial Tbx5 inactivation downregulated highly chamber specific genes such as Myl7 and Nppa, and increased expression of ventricular identity genes including Myl2. Using combined single nucleus transcriptome and open chromatin profiling, we assessed genomic accessibility changes underlying the altered atrial identity expression program, identifying 1846 genomic loci with greater accessibility in control atrial cardiomyocytes compared to KO aCMs. 69% of the control-enriched ATAC regions were bound by TBX5, demonstrating a role for TBX5 in maintaining genomic accessibility. These regions were associated with genes that had higher expression in control aCMs compared to KO aCMs, suggesting they act as TBX5-dependent enhancers. To confirm this hypothesis we analyzed chromatin looping of enhancers marked by H3K27Ac using HiChIP and found 510 chromatin loops that were sensitive to TBX5 dosage. Of the loops enriched in control aCMs, 73.7% contained anchors in control-enriched ATAC regions. Conversely, Tbx5 overexpression in the ventricular myocardium drove atrial gene expression. Together, these data demonstrate a role for TBX5 in maintaining the atrial gene expression program by binding to atrial enhancers to preserve tissue-specific chromatin architecture. We highlight this phenomenon at major atrial identity genes including Nppa, Bmp10 and Myl7.
2023-08-11 | GSE222373 | GEO
Project description:Understanding how the atrial and ventricular chambers of the heart maintain their distinct identity is a prerequisite for treating chamber-specific diseases. Here, we selectively inactivated the transcription factor Tbx5 in the atrial working myocardium of the neonatal mouse heart to show that it is required to maintain atrial identity. Atrial Tbx5 inactivation downregulated highly chamber specific genes such as Myl7 and Nppa, and increased expression of ventricular identity genes including Myl2. Using combined single nucleus transcriptome and open chromatin profiling, we assessed genomic accessibility changes underlying the altered atrial identity expression program, identifying 1846 genomic loci with greater accessibility in control atrial cardiomyocytes compared to KO aCMs. 69% of the control-enriched ATAC regions were bound by TBX5, demonstrating a role for TBX5 in maintaining genomic accessibility. These regions were associated with genes that had higher expression in control aCMs compared to KO aCMs, suggesting they act as TBX5-dependent enhancers. To confirm this hypothesis we analyzed chromatin looping of enhancers marked by H3K27Ac using HiChIP and found 510 chromatin loops that were sensitive to TBX5 dosage. Of the loops enriched in control aCMs, 73.7% contained anchors in control-enriched ATAC regions. Conversely, Tbx5 overexpression in the ventricular myocardium drove atrial gene expression. Together, these data demonstrate a role for TBX5 in maintaining the atrial gene expression program by binding to atrial enhancers to preserve tissue-specific chromatin architecture. We highlight this phenomenon at major atrial identity genes including Nppa, Bmp10 and Myl7.
2023-08-11 | GSE222579 | GEO
Project description:We Knocked out the TBX5 gene in iPSCs by TALEN-mediated NHEJ and report the gene expression in isogenic iPSC-CMs
2020-01-26 | GSE83657 | GEO
Project description:We deep sequenced wildtype and Tbx5-mutant mouse atria, identifying ~2600 novel Tbx5-dependent ncRNAs. Tbx5-dependent ncRNA transcription provided a quantitative metric of Tbx5-dependent enhancer activity, correlating with target gene expression.
2023-08-02 | GSE239805 | GEO
Project description:T-box transcription factors have been shown to play critical roles in the development and identity of the lungs. Tbx5 has been implicated as an initiator of pulmonary development through direct regulation of signaling molecules of the posterior second heart field (pSHF) and cardiopulmonary progenitors (CPs) (Arora et al. 2012 PLOS Genetics; Steimle et al 2018 PNAS). We hypothesize TBX5 regulates additional targets required for lung development. To this end, we performed ChIP-sequencing to identify localization of TBX5 during fetal lung development.
2021-02-23 | GSE167207 | GEO
Project description:Using an oligonucleotide-based microarray analysis to study the expression of special genes in tbx5 morphants, we demonstrated that GH and some GH-related genes were markedly downregulated. Two condition experiments, tbx5 morpholino vs. wilde-type control Danio rerio embryo.
2011-12-06 | E-GEOD-33965 | biostudies-arrayexpress
Project description:TBX5 overexpression in ventricle
| PRJNA922565 | ENA
Project description:T-box transcription factors play critical roles in the development and identity of the heart. Tbx5 has been implicated as a regulator of the fast-conducting, ventricular conduction system, while Tbx3 has been implicated as a regulator of the slow-conducting node. We hypothesize TBX5 and TBX3 share common binding sites in cardiomyocytes to positively or negatively regulate transcription, respectively, for cardiac cell identity and conduction. To this end, we performed ChIP-sequencing to identify localization of TBX5 during fetal heart development and have compared it with previously published histone (GEO Series: GSE31039; ENCODE Accessions: ENCSR080GQM, ENCSR000CDL, ENCSR000CDM, ENCSR052CDF, ENCSR345RKE, ENCSR007XTC, ENCSR360ANE, ENCSR000CDK, and ENCSR357OED) and TBX3 ChIP-seq (GSM862695).
2020-04-21 | GSE139803 | GEO