TBX5 ChIP from the Fetal Heart
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA587057 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10382543.fastq.gz | Fastqsanger.gz | |||
| SRR10382544.fastq.gz | Fastqsanger.gz | |||
| SRR10382545.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 3 of 3 |
Similar Datasets
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
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:Tbx5 is expressed in the left ventricle of the developing mammalian heart. In order to test the transcriptional requirement of Tbx5 in the fetal left ventricle and bypass its early requirement in early cardiac formation, we used a combination of the ROSA26creERT2, a ubiquitously transcribed tamoxifen-dependent cre recombinase, and the Tbx5 floxed allele to remove both copies of Tbx5 at E11.5 followed by microdissection at E12.5. In addition to several well-known targets of Tbx5, we identified a novel signature of disrupted PDGF signaling.
2022-12-16 | GSE125823 | GEO
Project description:To understand Tbx5-Hedgehog molecular networks in the posterior second heart field (pSHF), we have employed whole genome microarray expression profiling as a discovery platform to identify genes with Tbx5-dependent expression changes. We microdissected the pSHF from E9.5 embryos and compared the Tbx5 mutant samples with than of wild-type using Agilent 4x44k Mouse Whole Genome Arrays (n = 4 WT pools and 4 Tbx5 -/+ pools). Microdissected pSHF from E9.5 mouse embryos was molecularly verified by real-time PCR. Tbx5 mutant embryos were compared with wild-type embryos. Four independnet pools of RNAs from each biological group were measured on 1-color Agilent Mouse Whole Genome Arrays (n = 4 WT pools and 4 Tbx5 -/+ pools).
2013-02-08 | E-GEOD-43599 | biostudies-arrayexpress
Project description:To understand Tbx5-Hedgehog molecular networks in the posterior second heart field (pSHF), we have employed whole genome microarray expression profiling as a discovery platform to identify genes with Tbx5-dependent expression changes. We microdissected the pSHF from E9.5 embryos and compared the Tbx5 mutant samples with than of wild-type using Agilent 4x44k Mouse Whole Genome Arrays (n = 4 WT pools and 4 Tbx5 -/+ pools).
2013-02-08 | GSE43599 | GEO
Project description:The transcription factor FOG2 (ZFPM2) is upregulated in human heart failure and increased FOG2 expression causes heart failure in mice. We found that FOG2 directly intersects a gene regulatory network driven by the atrial-enriched TF TBX5 and required for atrial cardiomyocyte rhythm control gene expression
2024-05-02 | GSE198733 | 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. 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