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Expression data from GTF2i mutated ES cells

ABSTRACT: Data present the expression analysis of different mouse ES cell line with altered expression of GTF2I.

ORGANISM(S): Mus musculus

PROVIDER: GSE48790 | GEO | 2013/07/12

SECONDARY ACCESSION(S): PRJNA211729

REPOSITORIES: GEO

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Expression data from GTF2i mutated ES cells

Project description:Data present the expression analysis of different mouse ES cell line with altered expression of GTF2I. We used microarrays to detail the global programme of gene expression underlying altered expression of GTF2I and identified distinct classes of deregulated genes

2013-07-12 | E-GEOD-48790 | biostudies-arrayexpress

Expression data from inducible ES stable cell line overexpressing specifically the human gene GTF2I

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GTF2I mutation induces metabolic alterations and cell transformation in thymic epithelial cells [II]

Project description:The molecular mechanisms underlying the pathogenesis of TETs are poorly understood. Recently we reported a common missense mutation on GTF2I gene in thymic tumors and hypothesized that GTF2I mutation might contribute to thymic tumorigenesis. Expression of mutant TFII-I altered the transcriptome of thymic epithelial cells and up-regulated several oncogenic genes. Using CRISPR/Cas9n, Gtf2i T1211A knock-in cells exhibited distinct features of cancerous cells including cell transformation, aneuploidy, tumor growth in xenograft, and survival after DNA damage or glucose deprivation. We also observed that Gtf2i mutation increased the expression of several glycolytic enzymes, cyclooxygenase-2, and altered lipid metabolism. Elevated COX-2 expression by Gtf2i mutation was required for survival under metabolic stress and cellular transformation of thymic epithelial cells. Our findings identify GTF2I mutation as a new oncogenic driver mutation that is responsible for transformation of thymic epithelial cells.

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Project description:Individuals with Williams syndrome (WS), a multisystemic neurodevelopmental disorder, characteristically portray a hypersocial phenotype. WS is caused by the hemizygous loss of 26-28 genes at chromosomal locus 7q11.23, one of which is GTF2I. Copy number variations and mutations in GTF2I are associated with altered sociality and have been proposed to underlie the hypersocial expression of WS. However, the contribution of GTF2I to human neurodevelopment remains poorly understood. Here, human cellular models of neurodevelopment, including neural progenitors, neurons, and three-dimensional cortical organoids, were differentiated from CRISPR-Ca9-edited GTF2I-knockout (GTF2I-KO) pluripotent stem cells (hiPSCs) to investigate the role of GTF2I in human neurodevelopment. Compared to controls, GTF2I-KO progenitors exhibited an increased proliferation rate and an altered cell cycle profile. Cortical organoids and neurons demonstrated increased cell death and synaptic dysregulation, including synaptic structural dysfunction and decreased electrophysiological activity on a multi-electrode array. Overall, our findings suggest that changes in synaptic circuit integrity may be a prominent mediator of the link between alterations in GTF2I and variation in the phenotypic expression of human sociality.

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