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Genome-wide profiling of the Sox chondrogenic trio at E13.5

ABSTRACT: Transgenic mice tagged with EGFP under the control of the endogenous Sox5, Sox6 and Sox9 promoter were used. E13.5 transgenic embryos were enriched for the skeletal elements and FACS was used to isolate the Sox5/6/9-expressing cells which were used for comparative expression profiling between wildtype and knockout.

ORGANISM(S): Mus musculus

PROVIDER: GSE33173 | GEO | 2017/06/10

SECONDARY ACCESSION(S): PRJNA149221

REPOSITORIES: GEO

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In vivo genome-wide chromatin immunoprecipitation for the chondrogenic transcription factors, Sox9, Sox5 and Sox6

Project description:Tissue ChIP-seq was performed on transcription factor Sox5, Sox6 and Sox9 using limbs and tails from E13.5 mouse embryos to find their in vivo binding sites in the genome

2017-06-15 | GSE33419 | GEO

Transcription profiling of human mesenchymal stem cells transfected with adenoviruses carrying the SOX trio or LacZ control to identify target molecules

Project description:The aim of the experiment is to identify target molecules of the SOX trio (SOX9, SOX5 and SOX6). hMSC were transfected with the adenoviruses carrying the SOX trio or the LacZ-control, and total RNA was isolated after 2 weeks of culture.

2007-04-01 | E-MEXP-960 | biostudies-arrayexpress

RNA-seq data from mouse newborn rib chondrocytes

Project description:To understand the targets of Sox5, Sox6 and Sox9, we overexpressed Sox5/6/9 in mouse newborn rib chondrocytes and expression analysis by RNA-seq.

2021-01-20 | GSE155118 | GEO

The transcription factors SOX9 and SOX5/SOX6 cooperate genome-wide through super-enhancers to drive chondrogenesis (ChIP-Seq)

Project description:SOX9 is a transcriptional activator required for chondrogenesis, and SOX5 and SOX6 are closely related DNA-binding proteins that critically enhance its function. We used RNA-seq to charatierize a rat chondrosarcoma (RCS) cells as a faithful model for proliferating/early prehypertrophic growth plate chondrocytes and ChIP-seq to gain novel insights into the full spectrum of the target genes and modes of action of this chondrogenic trio. ChIP-seq for SOX9, SOX6 and histone modifications were carried out using RCS cells

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The protein kinase MLTK Is a key regulator for chondrogenesis.

Project description:Sox9 acts together with Sox5 or Sox6 as a master regulator for chondrocyte differentiation; however, how these transcription factors functionally interact and collaborate to regulate chondrogenesis remains unclear. Here we show that the protein kinase MLTK plays an essential role in the onset of chondrogenesis through triggering the induction of Sox6 by Sox9. Knockdown of MLTK in Xenopus embryos results in drastic loss of craniofacial cartilages without defects in neural crest formation. We also find that Sox6 is specifically induced during craniofacial chondrogenesis and this induction is inhibited by MLTK knockdown. Remarkably, Sox6-knockdown embryos display essentially the same phenotype as the MLTK-knockdown embryos; the drastic loss of cartilages and the marked down-regulation of genes involved in chondrogenesis. Microarray analysis reveals a remarkable similarity between Sox6-depleted and MLTK-depleted embryos in their gene expression pattern. Moreover, we find that ectopic expression of MLTK can induce Sox6 expression in a Sox9-dependent manner. These results identify a novel, key regulator for chondrogenesis. We used microarrays to describe the genome-wide gene expression profiles of xMLTK-depleted and xSox6-depleted embryos.

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Expression data of e13.5 Sox-GFP forming digit, e14.5 Lgr5-GFP+ interzone and e14.5 GFP- surrounding tissues in digit

Project description:Lgr5 is a novel marker expressing in the interzone from around e14.5 of developing synovial joint. By comparing the expression profiles of e14.5 Lgr5+ interzone cells, surrounding Lgr5- non-interzone cells and also e13.5 digit, we have identified some differential expressing genes in the interzone. We have generated bulk RNAseq data of e14.5 Lgr5+ interzone cells, surrounding non-interzone cells and e13.5 Sox9+ chondrocytes cells in digit.

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Sox5 and Sox6 direct a cardiac adaptive response to pressure overload

Project description:Rationale: We previously demonstrated that the transcription factor Sox6 regulates skeletal muscle biology by determining myofiber composition and muscle performance. Although the role of Sox6 and Sox5, its closest paralog, has not been ascertained in the heart, genome-wide association studies linked both Sox5 and Sox6 to cardiovascular disease. Objective: This study identifies the role of Sox5 and Sox6 in the adult mammalian heart under normal and stress conditions. Methods and Results: Using Sox5 and Sox6 cardiac-specific and Sox5 conduction system-specific knockout mice, we investigated the role of the two transcription factors in the heart under normal conditions and during cardiac stress. Sox5/6-deficient (DKO) mice displayed blunted cardiac contractility, which was present in Sox5 but not Sox6 single KO mice. DKO mice had a mild reduction in blood pressure, and conduction-specific knockout of Sox5 resulted in a reduced heart rate at baseline. After cardiac pressure overload, DKO mice showed increased lethality compared to control mice and were more prone to develop heart failure. We performed RNA deep sequencing in ventricles from DKO and control mice to identify potential Sox5/6 target genes and found altered expression of genes encoding regulators of calcium handling and cation transporters. Patch-clamping in isolated cardiomyocytes revealed shortened action potential duration in Sox5 KO cells. Conclusions: Unlike in skeletal muscle, our results suggest Sox5 but not Sox6 to be a major regulator of cardiac function and rhythm. Sox5 is essential to preserve cardiac function under normal conditions by maintaining contractility and to prevent cardiac failure after pressure overload.

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2015-06-23 | E-GEOD-70142 | biostudies-arrayexpress

The transcription factors SOX9 and SOX5/SOX6 cooperate genome-wide through super-enhancers to drive chondrogenesis (RNA-Seq)

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The transcription factors SOX9 and SOX5/SOX6 cooperate genome-wide through super-enhancers to drive chondrogenesis (ChIP-Seq)

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