Gallus gallus
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Similar Datasets
Project description:SOX9 ChIP-seq data of E13 mouse developing limb buds and male gonads
| PRJDB3815 | ENA
Project description:We used the RCAS avian retrovirus to overexpress SOCS2 in the developing chicken limb buds and transcriptome sequencing (mRNA-Seq) revealed changes in expression of genes known to be associated with growth and development in forelimbs with overexpressed SOCS2.
2024-04-17 | GSE252616 | GEO
Project description:miRNA profiling in male and female chicken embryonic gonads during sexual differentiation
| PRJNA109737 | ENA
Project description:Sox9 is an SRY-related transcription factor required for expression of cartilaginous matrix genes in the developing skeletal system and heart valve structures. In contrast to positively regulating formation of cartilaginous matrix, Sox9 has also been shown to negatively regulate matrix mineralization associated with bone formation. While the transcriptional activation of Sox9 target genes during chondrogenesis has been well studied, the mechanisms by which Sox9 represses osteogenic processs are not so clear. To address this, we performed a genome-wide Sox9 ChIP-on-chip approach using neonatal mouse lim tissue. Chromatin immunoprecipitation was performed with pooled Sox9 antibodies and normal rabbit IgG as control using neonatal mouse limb tissue. Samples include Sox9 IP and IgG IP.
2011-11-01 | E-GEOD-29058 | biostudies-arrayexpress
Project description:To define the repertoire of Sox9-dependent genes that contribute to the regulation of chondrogenesis, we generated Sox9-3'enhanced green fluorescent protein (EGFP) knock-in mice (Sox9-3'EGFP) and Sox9-EGFP/EGFP null chimeras. EGFP-positive cells of Sox9-3'EGFP knock-in and Sox9-EGFP/EGFP null chimeric embryos harvested from limb buds at embryonic day 12.5 were sorted using a FACSAria flow cytometer (Becton-Dickinson). Total RNA of sorted cells was extracted using the RNeasy Mini Kit (QIAGEN) and amplified according to the instructions provided by Affymetrix. Microarray analysis using the Affymetrix Mouse Genome 430 2.0 Array was performed according to the manufacturer's instructions.
2011-02-16 | E-MTAB-537 | biostudies-arrayexpress
Project description:Heart valve formation initiates when endothelial cells of the heart transform into mesenchyme and populate the cardiac cushions. The transcription factor, SOX9, is highly expressed in the cardiac cushion mesenchyme, and is essential for heart valve development. Loss of Sox9 in mouse cardiac cushion mesenchyme alters cell proliferation, embryonic survival, and disrupts valve formation. Despite this important role, little is known regarding how SOX9 regulates heart valve formation or its transcriptional targets. Therefore, we mapped putative SOX9 binding sites by ChIP-Seq in embryonic day (E) 12.5 heart valves, a stage at which the valve mesenchyme is actively proliferating and initiating differentiation. Embryonic heart valves have been shown to express a high number of genes that are associated with chondrogenesis, including several extracellular matrix proteins and transcription factors that regulate chondrogenesis. Consequently, we compared regions of putative SOX9 DNA-binding between E12.5 heart valves and E12.5 limb buds. We identified context-dependent and contextâindependent SOX9 interacting regions throughout the genome. Analysis of context-independent SOX9 binding suggests an extensive role for SOX9 across tissues in regulating proliferation-associated genes including key components of the AP-1 complex. Integrative analysis of tissue-specific SOX9 interacting regions and gene expression profiles on Sox9-deficient heart valves demonstrated that SOX9 controls the expression of several transcription factors with previously identified roles in heart valve development, including Twist1, Sox4, Mecom/Evi1 and Pitx2. Together, our data identifies SOX9 coordinated transcriptional hierarchies that control cell proliferation and differentiation during valve formation. Examination of SOX9 binding sites in E12.5 atrioventricular canal (AVC) and E12.5 embryonic limb and mRNA expression profiling in E12.5 WT and Sox9 mutant AVCs, in duplicate.
2015-11-05 | E-GEOD-73225 | biostudies-arrayexpress
Project description:The combinatorial expression of the Hox genes along the body axes, referred to as the HOX code, is a major determinant of cell fate and plays a prevailing role in generating the animal body plan. In developing limb buds, the paralogous group 13 genes of the HoxA and HoxD clusters are essential for patterning the distal-most limb structures, the digits. Inactivation of HOXA13 and HOXD13 transcription factors (HOX13) leads to complete digit agenesis in mice, but how HOX13 regulate transcriptional outcomes and confer identity to the distal-most limb cells has remained elusive. Here we performed genome-wide profiling of HOX13 by chromatin immunoprecipitation and analyzed the transcriptome and chromatin state of wild type early and late-distal limb buds, as well as Hoxa13-/-;Hoxd13-/- compound mutant limb buds. Our results show that inactivation of HOX13 impairs the activation and repression of putative cis-regulatory modules specific to the late-distal limb cells. Loss of HOX13 also disrupts the specific, spatial patterning of gene expression along the proximal-distal axis of the developing limb buds. These results show that proper termination of the early limb transcriptional program and activation of the late-distal limb program are coordinated by the dual action of HOX13 on cis-regulatory modules.
2016-12-14 | GSE81357 | GEO
Project description:The combinatorial expression of the Hox genes along the body axes, referred to as the HOX code, is a major determinant of cell fate and plays a prevailing role in generating the animal body plan. In developing limb buds, the paralogous group 13 genes of the HoxA and HoxD clusters are essential for patterning the distal-most limb structures, the digits. Inactivation of HOXA13 and HOXD13 transcription factors (HOX13) leads to complete digit agenesis in mice, but how HOX13 regulate transcriptional outcomes and confer identity to the distal-most limb cells has remained elusive. Here we performed genome-wide profiling of HOX13 by chromatin immunoprecipitation and analyzed the transcriptome and chromatin state of wild type early and late-distal limb buds, as well as Hoxa13-/-;Hoxd13-/- compound mutant limb buds. Our results show that inactivation of HOX13 impairs the activation and repression of putative cis-regulatory modules specific to the late-distal limb cells. Loss of HOX13 also disrupts the specific, spatial patterning of gene expression along the proximal-distal axis of the developing limb buds. These results show that proper termination of the early limb transcriptional program and activation of the late-distal limb program are coordinated by the dual action of HOX13 on cis-regulatory modules.
2016-12-14 | GSE81356 | GEO
Project description:The basic helix-loop-helix transcription factor Twist1 has a well-documented role in mesenchymal populations of the developing embryo, such as endocardial cushion (ECC) mesenchymal cells and limb buds, and during cancer development and progression. Whether Twist1 regulates the same transcriptional targets in different cell types has yet to be investigated. Through chromatin immunoprecipitation followed by sequencing (Chip-seq) analysis, the cell type-specific genome-wide occupancy of Twist1 was investigated in ECCs, limb buds and mouse peripheral nerve sheath tumor (PNST) cells. Twist1 binds mainly in a cell type-specific manner, with very few common genomic regions occupied by Twist1 in different cell types. Genes associated with binding peaks in each cell type are related to known Twist1 cellular functions in ECCs, limb buds, and cancer cells. We found that cell type-specific binding of Twist1 may be influenced by histone modifications or co-factors. Binding regions were located in several Wnt pathway associated genes, supporting a link between Twist1 and Wnt signalling in ECCs, limb buds, and PNST cells. These data suggest that similar functions are regulated by Twist1 in ECCs, limb buds, and PNST cells in a cell type-specific manner, and provide insights into possible mechanisms utilized for cell type-specificity of Twist1 binding. We compare Twist1 genome occupancy in mouse embryonic day (E) 12.5 endocardial cushion mesenchymal cells, E10.5 forelimb buds, and a mouse peripheral nerve sheath tumor cell line.
2014-10-02 | E-GEOD-50111 | biostudies-arrayexpress
Project description:The basic helix-loop-helix transcription factor Twist1 has a well-documented role in mesenchymal populations of the developing embryo, such as endocardial cushion (ECC) mesenchymal cells and limb buds, and during cancer development and progression. Whether Twist1 regulates the same transcriptional targets in different cell types has yet to be investigated. Through chromatin immunoprecipitation followed by sequencing (Chip-seq) analysis, the cell type-specific genome-wide occupancy of Twist1 was investigated in ECCs, limb buds and mouse peripheral nerve sheath tumor (PNST) cells. Twist1 binds mainly in a cell type-specific manner, with very few common genomic regions occupied by Twist1 in different cell types. Genes associated with binding peaks in each cell type are related to known Twist1 cellular functions in ECCs, limb buds, and cancer cells. We found that cell type-specific binding of Twist1 may be influenced by histone modifications or co-factors. Binding regions were located in several Wnt pathway associated genes, supporting a link between Twist1 and Wnt signalling in ECCs, limb buds, and PNST cells. These data suggest that similar functions are regulated by Twist1 in ECCs, limb buds, and PNST cells in a cell type-specific manner, and provide insights into possible mechanisms utilized for cell type-specificity of Twist1 binding.
2014-10-02 | GSE50111 | GEO