Mus musculus
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR031849_1.fastq.gz | Fastqsanger.gz | |||
| DRR031849_2.fastq.gz | Fastqsanger.gz | |||
| DRR031850_1.fastq.gz | Fastqsanger.gz | |||
| DRR031850_2.fastq.gz | Fastqsanger.gz | |||
| DRR031851_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
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Project description:SOX9 ChIP-seq data of E7 chicken developing limb buds and male gonads
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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:A major event in mammalian male sex determination is the induction of the testis determining factor Sry and its downstream gene Sox9. The current study provides one of the first genome wide analyses of the downstream gene binding targets for SRY and SOX9 to help elucidate the molecular control of Sertoli cell differentiation and testis development. A modified ChIP-Chip analysis using a comparative hybridization was used to identify 71 direct downstream binding targets for SRY and 109 binding targets for SOX9. Interestingly, only 5 gene targets overlapped between SRY and SOX9. In addition to the direct response element binding gene targets, a large number of atypical binding gene targets were identified for both SRY and SOX9. Bioinformatic analysis of the downstream binding targets identified gene networks and cellular pathways potentially involved in the induction of Sertoli cell differentiation and testis development. The specific DNA sequence binding site motifs for both SRY and SOX9 were identified. Observations provide insights into the molecular control of male gonadal sex determination. The current study provides one of the first genome wide analyses of the downstream gene binding targets for SRY and SOX9 to help elucidate the molecular control of Sertoli cell differentiation and testis development. At embryonic day 13 (E13) of pregnancy rats were euthanized and embryonic gonads were collected for chromatin. A modified ChIP-Chip analysis using a comparative hybridization was used to identify direct downstream binding targets for SRY and for SOX9. Then, bioinformatic analysis of the downstream binding targets was done to identify gene networks and cellular pathways that are potentially involved in the induction of Sertoli cell differentiation and testis development.
2014-12-05 | E-GEOD-63855 | biostudies-arrayexpress
Project description:A major event in mammalian male sex determination is the induction of the testis determining factor Sry and its downstream gene Sox9. The current study provides one of the first genome wide analyses of the downstream gene binding targets for SRY and SOX9 to help elucidate the molecular control of Sertoli cell differentiation and testis development. A modified ChIP-Chip analysis using a comparative hybridization was used to identify 71 direct downstream binding targets for SRY and 109 binding targets for SOX9. Interestingly, only 5 gene targets overlapped between SRY and SOX9. In addition to the direct response element binding gene targets, a large number of atypical binding gene targets were identified for both SRY and SOX9. Bioinformatic analysis of the downstream binding targets identified gene networks and cellular pathways potentially involved in the induction of Sertoli cell differentiation and testis development. The specific DNA sequence binding site motifs for both SRY and SOX9 were identified. Observations provide insights into the molecular control of male gonadal sex determination. The current study provides one of the first genome wide analyses of the downstream gene binding targets for SRY and SOX9 to help elucidate the molecular control of Sertoli cell differentiation and testis development. At embryonic day 13 (E13) of pregnancy rats were euthanized and embryonic gonads were collected for chromatin. A modified ChIP-Chip analysis using a comparative hybridization was used to identify direct downstream binding targets for SRY and for SOX9. Then, bioinformatic analysis of the downstream binding targets was done to identify gene networks and cellular pathways that are potentially involved in the induction of Sertoli cell differentiation and testis development.
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Project description:We report time-series transcriptome of developing bamboo shark fin buds and mouse forelimb buds, and open chromatin regions of developing mouse forelimb buds. The major contributions of this study are 1) transcriptomic data with an accurate orthology map for a systematic comparison between the two species; 2) high quality chromatin accessibility data for mouse limb development; 3) discovery of mass heterochronic genes between fins and limbs; 4) hourglass-shaped conservation between fins and limbs, providing insights into a general trend of gene regulatory evolution.
2019-09-17 | GSE136437 | GEO
Project description:We report time-series transcriptome of developing bamboo shark fin buds and mouse forelimb buds, and open chromatin regions of developing mouse forelimb buds. The major contributions of this study are 1) transcriptomic data with an accurate orthology map for a systematic comparison between the two species; 2) high quality chromatin accessibility data for mouse limb development; 3) discovery of mass heterochronic genes between fins and limbs; 4) hourglass-shaped conservation between fins and limbs, providing insights into a general trend of gene regulatory evolution.
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2014-10-02 | E-GEOD-50111 | 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.
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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: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.
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