Rat Schwann cell gene expression analysis after Sox2 overexpression
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ABSTRACT:
PROVIDER: PRJNA510314 | ENA |
REPOSITORIES: ENA
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Project description:In this dataset, we include the expression data obtained from rat Schwann cells overepressing GFP (control) or Sox2/GFP to identfiy Sox2 tragets in Schwann cells. An in vitro microarray analysis of GFP (control) and Sox2/GFP overexpressing Schwann cells
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Project description:The extracellular matrix is essential for tissue formation and regeneration through the control of cellular behavior. Deregulation of extracellular matrix components is associated to disease, including neurodegeneration. After peripheral nerve injury, Schwann cells guide regrowing axons to their targets. These glial cells migrate collectively and provide an extracellular environment to enable neural repair. How this occurs remains poorly understood. Here, we show that Sox2 controls fibronectin fibrillogenesis in Schwann cells to provide a highly oriented extracellular matrix, which supports their rapid collective migration with a continuous cellular flow. Sox2 directly activates fibronectin expression in Schwann cells, leading to an increase in fibrillogenesis and cellular huddling. Accordingly, loss of fibrillogenesis leads to glial disassembly and disorganized axon regrowth. In vivo, 7 days post nerve injury, we found that pro-regenerative Schwann cells co-express Sox2 and the EIIIA-containing fibronectin splicing isoform. This mechanism is conserved in mammals, including humans, but absent in zebrafish. Taken together, our results demonstrate that Sox2 directly controls fibrillogenesis and provide a novel mechanism for the modification of the environmental architecture by glial cells during neuronal repair.
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Project description:We utilized RNA-Seq on rat Schwann (S16) cells to determine global gene expression. This information was generated as part of a larger effort to characterize cis-regulatory elements and global gene expression within Schwann cells. To achieve this, we generated RPKM values across two independent biological replicates. This dataset was also used to predict cis-regulatory element function on genes following CRISPR knockout studies.
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Project description:In order to understand the molecular mechanisms of changes seen in the adult mouse intestine in response to Sox2 overexpression, gene expression was analyzed in the ileum upon 2-day Doxycycline (DOX) treatment of mice containing Dox-inducible Sox2 transgene. Repression of Cdx2 and of its intestinal targets was observed and confirmed by Western blotting and immunostaining. This effect of Sox2 was distinct from the effect of overexpression of Oct4. 6-8 week old TetON-Sox2, rtTA controls (no TetOP-Sox2 transgene), TetON-Oct4, and TetON-Sox2 X TetON-Oct4 mice (2 replicates) were treated for 2 days with 2 mg/ml DOX or were left untreated. Intestines (ileum part) were collected and total mRNA was extracted.
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Project description:In order to understand the molecular mechanisms of changes seen in the adult mouse intestine in response to Sox2 overexpression, gene expression was analyzed in the ileum upon 2-day Doxycycline (DOX) treatment of mice containing Dox-inducible Sox2 transgene. Repression of Cdx2 and of its intestinal targets was observed and confirmed by Western blotting and immunostaining. This effect of Sox2 was distinct from the effect of overexpression of Oct4.
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Project description:Transcriptional profiling of adult forestomach epithelium comparing K5-CreER controsl with K5-CreER;Rosa26Sox2/Sox2 mutants. Two doses of tamoxifen were given and four weeks later the epithelal sheets were harvested for RNA extraction. Goal was to determine the effects of Sox2 overexpression on epithelial phenotypic changes. Two-condition experiment, wildtype Vs Sox2 overexpression mutant. Biological replicates: 3 control replicates, 3 mutant replicates.
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Project description:The transcription factor Sox2 inhibits human gastric cancer growth and activates Sox2-related tumor surpressive genes in human gastric cancer cells. Conditional Sox2-overexpression in cells with a low Sox2 level demonstrated that the Sox2-regulated tumor surpressive genes demand on an enhanced Sox2 activity for better expression to work in human gastric cancer. Chromatin immunoprecipitation (ChIP) of Sox2 together with chromatin profiling by ChIP-on-chip analysis demonstrated that Sox2 directly activates the chromatin at promoters or putative enhancers of Sox2 target genes. Transcription factor Sox2 promoter array in MKN28 cells with Sox2 overexpression.
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