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Tbx5 regulatory element controls atrial function and heart size [RNA-Seq]

ABSTRACT: Right and left ventricles RNA-seq of Tbx5(REint)-/- and control E14.5 mice (n=5)

ORGANISM(S): Mus musculus

PROVIDER: GSE168014 | GEO | 2023/02/10

REPOSITORIES: GEO

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Tbx5 regulatory element controls atrial function and heart size II

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Tbx5 regulatory element controls atrial function and heart size [ATAC-Seq]

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Tbx5 regulatory element controls atrial function and heart size

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Left-right transcriptomic differences in adult male mouse heart ventricles

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2013-03-21 | E-GEOD-45348 | biostudies-arrayexpress

Left-right transcriptomic differences in adult male mouse heart ventricles

Project description:Left and right heart ventricles of adult male mice were profiled to determine the differences in gene expression, control, coordination and signaling fabrics

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Tbx5-dependent transcripts of the embryonic left ventricle

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.

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TBX5 G125R induces profound transcriptional deregulation and atrial dysfunction in vivo [CUT&RUN]

Project description:Rationale: Pathogenic variants in the gene for T-box transcription factor (TF) 5 (TBX5) cause Holt-Oram syndrome (HOS), characterized by congenital heart defects and limb abnormalities. A particular missense variant in TBX5 (G125R) in a Dutch family causes atypical HOS as well as early onset atrial fibrillation (AF). Understanding the effects of such an altered key cardiac TF on the transcription regulatory network and cardiac physiology provides a unique opportunity to gain insight into the mechanisms underlying diseases such as AF. Objective: To determine the in vivo TBX5-G125R-induced changes in the transcriptional regulatory network and epigenetic state underlying the atypical HOS with early onset AF found in an extended pedigree. Methods and Results: We modeled the TBX5-G125R pathogenic variant in vivo in the mouse and found severe cardiac defects and fetal lethality in Tbx5G125R/G125R mice, whereas Tbx5G125R/+ mice were viable and morphologically unaffected. Electrophysiological analysis of adult Tbx5G125R/+ mice revealed variable RR interval, atrial extra systole and susceptibility to AF upon pacing. These characteristics were also observed in the patient family. Additionally, calcium homeostasis as well as conduction were changed in the mutant atrial cardiomyocytes. Single-nucleus transcriptional profiling of right atria revealed the most profound changes in expression in the cardiomyocytes of Tbx5G125R/+ mice. Transcriptional profiling of atrial tissue identified differential expression of over a thousand genes, whereas expression levels of several genes known to respond to Tbx5 insufficiency did not change. Epigenetic profiling revealed shifts in sites associated with acetylated H3K27 as well as in chrom atin accessibility in Tbx5G125R/+ atrial cardiomyocytes indicating Tbx5-G125R has altered DNA binding and TF interaction properties.

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