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TETs Regulate Proepicardial Cell Migration through Extracellular Matrix Organization during Zebrafish Cardiogenesis

ABSTRACT: TETs Regulate Proepicardial Cell Migration through Extracellular Matrix Organization during Zebrafish Cardiogenesis

PROVIDER: PRJNA501891 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8137050_1.fastq.gz	Fastqsanger.gz
	SRR8137050_2.fastq.gz	Fastqsanger.gz
	SRR8137051_1.fastq.gz	Fastqsanger.gz
	SRR8137051_2.fastq.gz	Fastqsanger.gz
	SRR8137042_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

TETs Regulate Proepicardial Cell Migration through Extracellular Matrix Organization during Zebrafish Cardiogenesis.

Project description:Ten-eleven translocation (Tet) enzymes (Tet1/2/3) mediate 5-methylcytosine (5mC) hydroxylation, which can facilitate DNA demethylation and thereby impact gene expression. Studied mostly for how mutant isoforms impact cancer, the normal roles for Tet enzymes during organogenesis are largely unknown. By analyzing compound mutant zebrafish, we discovered a requirement for Tet2/3 activity in the embryonic heart for recruitment of epicardial progenitors, associated with development of the atrial-ventricular canal (AVC). Through a combination of methylation, hydroxymethylation, and transcript profiling, the genes encoding the activin A subunit Inhbaa (in endocardium) and Sox9b (in myocardium) were implicated as demethylation targets of Tet2/3 and critical for organization of AVC-localized extracellular matrix (ECM), facilitating migration of epicardial progenitors onto the developing heart tube. This study elucidates essential DNA demethylation modifications that govern gene expression changes during cardiac development with striking temporal and lineage specificities, highlighting complex interactions in multiple cell populations during development of the vertebrate heart.

| S-EPMC6366638 | biostudies-literature

TETs Regulate Proepicardial Cell Migration through Extracellular Matrix Organization during Zebrafish Cardiogenesis

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-01-15 | GSE121991 | GEO

Ablation of collagen XII disturbs joint extracellular matrix organization and causes patellar subluxation

Project description:Ablation of collagen XII disturbs joint extracellular matrix organization and causes patellar subluxation

| PRJNA983815 | ENA

Mouse transcriptomics reveals extracellular matrix organization as a major pathway involved in inflammatory and neuropathic pain

Project description:Chronic pain is a debilitating and poorly-treated condition. The mechanisms underlying the development of chronic pain are not well understood. Nerve injury and inflammation cause alterations in gene expression in tissues associated with transmission of pain, supporting molecular and cellular mechanisms that maintain painful states. Previous studies in animal models and human patients suffering from different chronic pain conditions have examined changes in transcriptome associated with chronic pain. However, in most studies, the analyses were restricted to a single tissue or pain condition. In the current study, we performed next-generation sequencing of dorsal root ganglia, spinal cord, brain and blood in mouse models of nerve injury and inflammation-induced chronic pain. Comparative analyses of differentially expressed genes (DEG) across these tissues in two pain models identified the extracellular matrix organization (ECMO) pathway as the most commonly affected pathway. Interestingly, examination of GWAS datasets revealed an over-representation of DEGs within the ECMO pathway in SNPs most strongly associated with human back pain. Remarkably, manipulation of the extracellular matrix in the mouse significantly affected the development of pain hypersensitivity following nerve injury, supporting our gene expression findings. In summary, our comprehensive analysis of transcriptional landscape across different mouse pain models and tissues as well as human GWAS datasets identified extracellular matrix organization as a central molecular pathway in the development of chronic pain.

2019-04-04 | GSE111216 | GEO

Dysregulation of cell migration by matrix metalloproteinases in geleophysic dysplasia

Project description:Dysregulation of cell migration by matrix metalloproteinases in geleophysic dysplasia

| PRJNA1240284 | ENA

Dysregulation of cell migration by matrix metalloproteinases in geleophysic dysplasia

Project description:Geleophysic dysplasia (GD) is characterized by short stature, brachydactyly, joint limitations, a distinctive facial appearance, as well as cardiac and respiratory dysfunction that can be life-threatening. GD is caused by pathogenic variants in the ADAMTSL2, FBN1, or LTBP3 genes. While dermal fibroblasts derived from affected individuals have shown poor organization of the extracellular matrix (ECM), it remains elusive how the disorganized ECM contributes to GD pathogenesis. To understand the molecular mechanisms in GD, we isolated and characterized primary human dermal fibroblasts from affected individuals with ADAMTSL2 and FBN1 variants. We found that the secretion of ECM proteins including ADAMTSL2, FBN1, and Fibronectin were impaired in GD fibroblasts. Increased cell migration was observed in GD fibroblasts carrying ADAMTSL2 or FBN1 variants, which was associated with up-regulation of MMP-1 and MMP-14, two proteases related to cell mobility. The enhanced cell migration and up-regulation of MMP-1 and MMP-14 were corroborated in mouse primary dermal fibroblasts carrying pathogenic variants in Adamtsl2 and in lung and heart tissues from Adamtsl2-knockout mice. A pan MMP inhibitor, GM6001, inhibited the migration of GD fibroblasts. Overall, our results suggest that MMP-1/-14 up-regulation play a role in the development of GD and may be utilized as a treatment target.

2025-06-16 | GSE292600 | GEO

Elf3 deficiency during zebrafish development alters extracellular matrix organization and disrupts tissue morphogenesis.

Project description:E26 transformation specific (ETS) family transcription factors are expressed during embryogenesis and are involved in various cellular processes such as proliferation, migration, differentiation, angiogenesis, apoptosis, and survival of cellular lineages to ensure appropriate development. Dysregulated expression of many of the ETS family members is detected in different cancers. The human ELF3, a member of the ETS family of transcription factors, plays a role in the induction and progression of human cancers is well studied. However, little is known about the role of ELF3 in early development. Here, the zebrafish elf3 was cloned, and its expression was analyzed during zebrafish development. Zebrafish elf3 is maternally deposited. At different developmental stages, elf3 expression was detected in different tissue, mainly neural tissues, endoderm-derived tissues, cartilage, heart, pronephric duct, blood vessels, and notochord. The expression levels were high at the tissue boundaries. Elf3 loss-of-function consequences were examined by using translation blocking antisense morpholino oligonucleotides, and effects were validated using CRISPR/Cas9 knockdown. Elf3-knockdown produced short and bent larvae with notochord, craniofacial cartilage, and fin defects. The extracellular matrix (ECM) in the fin and notochord was disorganized. Neural defects were also observed. Optic nerve fasciculation (bundling) and arborization in the optic tectum were defective in Elf3-morphants, and fragmentation of spinal motor neurons were evident. Dysregulation of genes encoding ECM proteins and matrix metalloprotease (MMP) and disorganization of ECM may play a role in the observed defects in Elf3 morphants. We conclude that zebrafish Elf3 is required for epidermal, mesenchymal, and neural tissue development.

| S-EPMC9668168 | biostudies-literature

Mechanoresponsive genomic enhancers potentiate the cellular response to matrix stiffness [migration]

Project description:Mechanoresponsive genomic enhancers potentiate the cellular response to matrix stiffness [migration]

| PRJNA1019770 | ENA

Specific extracellular matrix remodeling signature of colon hepatic metastases

Project description:To identify genes implicated in metastatic colonization of the liver in colorectal cancer, we collected pairs of primary tumors and hepatic metastases before chemotherapy in 13 patients. We compared mRNA expression in the pairs of patients to identify genes deregulated during metastatic evolution. We then validated the identified genes using data obtained by different groups. The 33-gene signature was able to classify 87% of hepatic metastases, 98% of primary tumors, 97% of normal colon mucosa, and 95% of normal liver tissues in six datasets obtained using five different microarray platforms. The identified genes are specific to colon cancer and hepatic metastases since other metastatic locations and hepatic metastases originating from breast cancer were not classified by the signature. Gene Ontology term analysis showed that 50% of the genes are implicated in extracellular matrix remodeling, and more precisely in cell adhesion, extracellular matrix organization and angiogenesis. Because of the high efficiency of the signature to classify colon hepatic metastases, the identified genes represent promising targets to develop new therapies that will specifically affect hepatic metastasis microenvironment. 57 samples of patients with stage IV colorectal cancer. We compared using Affymetrix chips gene expression profiles between primary tumors and hepatic metastases

2013-09-01 | E-GEOD-49355 | biostudies-arrayexpress

LaminB and H3K9me2 ChIP-seq During Mouse Cardiogenesis

Project description:Progenitor cells require coordinated expression of lineage-specific programs, and the nuclear lamina has emerged as an important scaffold for organizing chromatin in many cell types. These ChIP-seq experiments accompany a study focused on defining nuclear organization changes during cardiac development. Specifically, these experiments map the binding sites of LaminB (a key nuclear lamina protein) and H3K9me2 (a histone modification enriched at the nuclear periphery) in mouse ESCs and ESC-derived cardiac myocytes. The observations of these experiments, within the context of the study, indicate that changes in the organization of key genes and cell-type specific genes occurs during cardiogenesis.

2017-10-12 | GSE97877 | GEO

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