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Posterior Second Heart Field (pSHF) Transcriptomes of Wild-type and Tbx5 Mutant Mouse Embryos

ABSTRACT: 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).

ORGANISM(S): Mus musculus

PROVIDER: GSE43599 | GEO | 2013/02/08

SECONDARY ACCESSION(S): PRJNA186796

REPOSITORIES: GEO

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Posterior Second Heart Field (pSHF) Transcriptomes of Wild-type and Tbx5 Mutant Mouse Embryos

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

Posterior Second Heart Field (pSHF) transcriptomes of wild-type and Shh mutant mouse embryos

2013-03-01 | GSE44754 | GEO

Posterior Second Heart Field (pSHF) transcriptomes of wild-type and Shh mutant mouse embryos

Project description:To understand Sonic hedgehog homolog (Shh)-mediated 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 Shh-dependent expressional changes. We microdissected the pSHF from E9.5 embryos and compared the Shh mutant samples with than of wild-type using Agilent 4x44k Mouse Whole Genome Arrays (n = 4 WT pools and 4 Shh - /- pools). Microdissected pSHF from E9.5 mouse embryos was molecularly verified by real-time PCR. Shh 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 = 3 WT pools and 4 Shh -/- pools).

2013-03-01 | E-GEOD-44754 | biostudies-arrayexpress

TBX5 ChIP from the Fetal Lung

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

Effect of histone deacetylase 3 (Hdac3) deficiency in second heart field on embryonic heart development.

Project description:Analysis of whole heart samples from Hdac3-Isl1KO embryos at embryonic day E9.5. Results provide insights into the role of Hdac3 in second heart field-derived cardiac cells. We used microarray to investigate the gene expression program affected by Hdac3 during cardiac development and identified patterns of differentially-expressed genes and pathways during this process.

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TBX5 KO HiChIP

Project description:TBX5 KO HiChIP

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Project description:TBX5 KO multiome

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TBX5 KO multiome

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

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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.

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