Similar Datasets
Project description:TBX5 removed from adult mice with R26CreERt2, right atrial RNA extracted and sequenced.
2023-08-02 | GSE239809 | GEO
Project description:TBX5 Adult Knockout Atrial Gene Expression
| PRJNA531601 | ENA
Project description:Left atrial RNA-seq of Tbx5(REint), Tbx5(REdown), Tbx5(Reint);Prrx1(RE) and control adult mice
2023-02-10 | GSE189342 | GEO
Project description:The left atrium consists of three major parts: the peri-pulmonary vein portion, the appendage, and the vestibule. Previous transcriptional profiling of the adult left atrium and identification of the Tbx5-dependent transcriptome has focused on the atrial appendage (Nadadur et al 2016, Science Translational Medicine). In that study, Tbx5 was shown to regulate a gene regulatory network of atrial identity in the appendage and in its absence results in atrial fibrillation. In order to investigate the regional differences in the transcriptome of the left atrium, the left atrial appendage and the peri-pulmonary vein portion from adult mice were compared by RNA-sequencing. Additionally, as Tbx5 is major regulator of atrial identity, the peri-pulmonary vein portion of the atria was likewise examined following removal of Tbx5 using an adult specific conditional knockout of Tbx5.
2020-03-10 | GSE128870 | GEO
Project description:Right and left ventricles RNA-seq of Tbx5(REint)-/- and control E14.5 mice (n=5)
2023-02-10 | GSE168014 | 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:Next Generation RNA Sequencing was carried out on human paired left and right atrial appendages from patients with and without Atrial Fibrillation. EdgeR software was used to show a total of 247 genes were found to have significant differential expression between left and right atria.
2019-03-13 | GSE128188 | GEO
Project description:The right and left atria have different susceptibilities towards developing arrhythmias, with left atrial arrhythmias more commonly observed. To study potential underlying causes of this difference between the two upper chambers of the heart, four human left-right atrial pairs were subjected to whole-genome expression analyses via next generation sequencing of small RNAs, including microRNAs (miRNAs), and polyA enriched mRNAs. Using a paired sample design, significant differences in gene expression were found between the left and right atria in both the poly-A and small RNA fractions. Hsa-miR-143 was the most highly expressed miRNA in the atria as quantified by RNA-seq. Gene expression differences established during development are retained into adulthood including that of PITX2 and BMP10. In addition ten novel non-coding RNAs were found to be differentially expressed between the left and right atrias .
2011-09-10 | GSE31999 | GEO
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.
2022-02-07 | GSE167081 | GEO
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.
2022-02-07 | GSE166971 | GEO