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ATAC-seq on endothelial cells from E11.5 mouse hearts

ABSTRACT: ATAC-seq on endothelial cells from E11.5 mouse hearts

PROVIDER: PRJEB11459 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1079313_1.fastq.gz	Fastqsanger.gz
	ERR1079313_2.fastq.gz	Fastqsanger.gz
	ERR1079314_1.fastq.gz	Fastqsanger.gz
	ERR1079314_2.fastq.gz	Fastqsanger.gz
	ERR1999764_1.fastq.gz	Fastqsanger.gz

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ChIP-seq of Tbx20 tagged with GFP in E11.5 mouse hearts

Project description:ChIP-seq of Tbx20 tagged with GFP in E11.5 mouse hearts

| PRJEB11457 | ENA

ATAC-seq on endocardial cells from E12.5 mouse hearts in Tbx20 knockouts and wild type counterparts

Project description:We used ATAC-seq (Buenrostro et al, 2013) to identify regions of open chromatin in FACS sorted mouse endothelial cells from E12.5 hearts. Please note that the animals were injected at different dates, which resulted in different effects of the knockout, as indicated in the batch attribute of the samples. This data set is part of the study \Endocardial Tbx20 is essential for mesenchymal and myocardial cell movements required for cardiac septation\. Peaks were called using HOMER (-gsize 1.87e9 -region -tbp 1). Replicate 1: -fdr 1e-8, replicate 2: default parameters. Buenrostro JD, Giresi PG, Zaba LC, Chang HY, Greenleaf WJ. 2013. Transposition of native chromatin for fast and sensitive epigenomic profiling of open chromatin, DNA-binding proteins and nucleosome position. Nat Methods 10: 12138.

2017-06-02 | E-MTAB-3972 | biostudies-arrayexpress

The chromatin accessibility in mouse pancreatic epithelial cells at E11.5, E13.5 and E15.5 during embryogenesis [ATAC-seq]

Project description:To understand the chromatin accessibility in mouse pancreatic epithelial cells at different stages during fetal development, we performed ATAC-seq in epithelial cells sorted from the pancreas tissues of E11.5, E13.5 and E15.5

2023-12-22 | GSE218736 | GEO

Genome-wide analysis of epicardial gene expression in E11.5 mouse hearts

Project description:Identification of epicardium-enriched genes in the embryonic heart. The epicardium encapsulates the heart and functions as a source of multipotent progenitor cells and paracrine factors essential for cardiac development and repair. Injury of the adult heart results in re-activation of a developmental gene program in the epicardium, but the transcriptional basis of epicardial gene expression has not been delineated. We established a mouse embryonic heart organ culture and gene expression system that facilitated the identification of epicardial enhancers activated during heart development and injury. Epicardial activation of these enhancers depends on a combinatorial transcriptional code centered on CCAAT/enhancer binding protein (C/EBP) transcription factors. Disruption of C/EBP signaling in the adult epicardium reduced injury-induced neutrophil infiltration and improved cardiac function. These findings reveal a transcriptional basis for epicardial activation and heart injury, providing a platform for enhancing cardiac regeneration. Total RNA obtained from lacZ-positive epicardial cells isolated from the E11.5 Tcf21lacZ hearts compared to total dissociated heart cells

2012-11-01 | E-GEOD-41959 | biostudies-arrayexpress

Expression data from Shox2 knockout and wildtype right atria of E11.5 mouse hearts

Project description:The heartM-bM-^@M-^Ys rhythm is initiated and regulated by a group of specialized cells in the sinoatrial node (SAN), the primary pacemaker of the heart. Abnormalities in the development of the SAN can result in irregular heart rates (arrhythmias). Although several of the critical genes important for SAN formation have been identified, our understanding of the transcriptional network controlling SAN development remains at a relatively early stage. The homeodomain transcription factor Shox2 plays an essential early role in the specification and patterning of the SAN. Here, we compared gene expression levels in the right atria of wildtype and Shox2-/- hearts using microarray experiments to identify Shox2 target genes. Right atria of E11.5 mouse embryos were dissected and genotyped for RNA extraction. RNA from 6 embryos and 2 independent pregnancies was pooled per genotype (Wildtype and Shox2 Knockout) and compared.

2013-06-03 | E-GEOD-39924 | biostudies-arrayexpress

ATAC-seq of E10.5 WT and Chd4-CMko mouse hearts

Project description:ATAC-seq of E10.5 WT and Chd4-CMko mouse hearts

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ATAC-seq of E9.5 WT and Smyd1-KO mouse hearts

Project description:ATAC-seq of E9.5 WT and Smyd1-KO mouse hearts

| PRJNA1082682 | ENA

Single-cell RNA-sequencing of angioblasts and endothelial cells from E9.5-E11.5 mouse embryos

Project description:Background: The formation of the lymphatic system has been a subject of controversy for over a century. Although the accepted view is that lymphatic endothelial cells originate exclusively from veins, there have been reports of non-venous derived lymphatics in multiple tissues. Methods: We performed single-cell RNA sequencing analyses on ~20000 individual cells isolated from Pax3Cre/+;Rosa26tdTomato mouse embryos at E9.5, E10.5 and E11.5, the temporal window in which lymphatic endothelium initially emerges. Results: These analyses revealed the existence of populations of lymphangioblasts which arise from paraxial mesoderm and directly incorporate into the lymph sacs. Our findings support the notion that lymphatic endothelial cells also have non-venous origins and explain the discrepancies between previous studies.

2024-10-18 | GSE276281 | GEO

ATAC-seq of E9.5 WT and Smyd1-KO mouse hearts

Project description:Purpose: The goal of this study is to identify the differential cardiac chromatin accessibility between WT and Smyd1 null (Smyd1-KO) hearts at E9.5 using ATAC-seq. Methods: Four hearts at E9.5 were pooled per genotype per replicate, and were then dissociated into single cells. 40,000 viable cells were taken for were lysed to isolate nuclei, which were treated with Tn5 transposase (Nextera DNA Sample Prep Kit, Illumina) to isolate DNA. Fragmented DNA was then amplified using bar-coded PCR primers and libraries were seuqenced. Results: 25851 differential peaks (2-fold change) were identified between E9.5 WT and Smyd1-KO hearts.

2024-04-18 | GSE260690 | GEO

ATAC-seq of E10.5 WT and Chd4-CMko mouse hearts

Project description:Purpose: The goal of this study is to identify the differential cardiac chromatin accessibility between WT and cardiomyocyte conditional knockout (Chd4-CMko) hearts at E10.5 using ATAC-seq. Methods: Three hearts at E10.5 were pooled per genotype per replicate, and were then dissociated into single cells. 40,000 viable cells were taken for were lysed to isolate nuclei, which were treated with Tn5 transposase (Nextera DNA Sample Prep Kit, Illumina) to isolate DNA. Fragmented DNA was then amplified using bar-coded PCR primers and libraries were seuqenced. Results: 15736 differential peaks (2-fold change) were identified between E10.5 WT and Chd4-CMko hearts.

2024-04-18 | GSE260689 | GEO

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