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| Status |
Public on Nov 05, 2015 |
| Title |
SOX9 modulates the expression of key transcription factors required for heart valve development |
| Organism |
Mus musculus |
| Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
Expression profiling by high throughput sequencing
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| Summary |
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 context–independent 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.
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| Overall design |
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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| Contributor(s) |
Hoodless PA, Cullum R, Garside VC |
| Citation(s) |
26525672 |
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| Submission date |
Sep 20, 2015 |
| Last update date |
May 15, 2019 |
| Contact name |
Pamela A. Hoodless |
| E-mail(s) |
hoodless@bccrc.ca
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| Phone |
(604) 675-8133
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| Organization name |
BC Cancer Agency
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| Department |
Terry Fox Laboratories
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| Lab |
Dr. Hoodless
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| Street address |
675 West 10th Avenue
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| City |
Vancouver |
| State/province |
British Columbia |
| ZIP/Postal code |
V5Z1L3 |
| Country |
Canada |
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| Platforms (2) |
| GPL9250 |
Illumina Genome Analyzer II (Mus musculus) |
| GPL16417 |
Illumina MiSeq (Mus musculus) |
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| Samples (5)
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| Relations |
| BioProject |
PRJNA296564 |
| SRA |
SRP063968 |
| Supplementary file |
Size |
Download |
File type/resource |
| GSE73225_RAW.tar |
260.0 Kb |
(http)(custom) |
TAR (of BED) |
| GSE73225_WT_versus_Sox9cKO_FPKMs_and_Fold_Change_merged_duplicates.txt.gz |
374.2 Kb |
(ftp)(http) |
TXT |
SRA Run Selector |
| Raw data are available in SRA |
| Processed data provided as supplementary file |
| Processed data are available on Series record |
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