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Dissecting developmental disorders caused by CTCF mutation at R567 [RNA-seq]

ABSTRACT: In this study, we analyzed gene expression change in brain tissues, in vitro cultured neurons and cortical organoids by using RNA-seq.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE214689 | GEO | 2024/05/06

REPOSITORIES: GEO

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Dissecting developmental disorders caused by CTCF mutation at R567

Project description:This SuperSeries is composed of the SubSeries listed below.

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Dissecting developmental disorders caused by CTCF mutation at R567 [4C]

Project description:In this study, we performed 4C sequencing experiments to investigate the change of chromatin interactions between the promoters of Pcdh genes and enhancers across cPcdh locus.

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Dissecting developmental disorders caused by CTCF mutation at R567 [Hi-C]

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Dissecting developmental disorders caused by CTCF mutation at R567 [SPARC-seq]

Project description:In this study, we performed SPARC-seq experiments in brain tissue from E18.5 mouse embryo.

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CTCF mutation at R567 causes developmental disorders by 3D genome rearrangement, premature exhaustion of stem cells and abnormal neurodevelopment [scRNA-seq]

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Proteomics characterisation of induced pluripotent stem cells and cortical brain organoids.

Project description:A method was developed to reproducibly produce neural retina and cortical brain regions from confluent cultures of stem cells. The spontaneously generated cortical organoids were isolated and cultured in suspension conditions for maturation. Proteomic analysis of both the original induced pluripotent stem cells and the cortical organoids demonstrated the increased presence of synaptic components, indicating maturity.

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Genetics of human developmental brain disorders

Project description:<p>Developmental brain malformations are at the core of significant neurological diseases affecting many families in the United States and around the world. It is known that epilepsy, specific learning deficits and intellectual disability, cerebral palsy, and abnormalities of brain volume can be attributed in many cases to pathological malformations of the cerebral cortex. Although these consequences, such as epilepsy and intellectual disability, might appear broadly in the population as due to complex traits, this study's focus on those associated with cortical malformations highlights individual developmental pathways likely represented by innumerable and rare Mendelian alleles. Research has thus far uncovered dozens of genes responsible for these conditions and dissected the mechanisms underlying early cortical development in animals. However, this progress represents only the dawn of understanding the complex genetic network and neuronal architecture of the uniquely human cerebral cortex.</p> <p>The overall goal of this study is to define the genetic bases of human cerebral cortical development. This is accomplished through (1) the ascertainment of families with disorders of human brain development and malformation, (2) categorizing these using medical, physical and neuroimaging data, and (3) mapping and identifying the gene causing the disorder of cortical development, which can then be investigated for its normal expression and function, and role in human disease.</p>

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Single cell analysis of iPSC-derived cortical organoids in biofunctionalized gelatin hydrogels

Project description:Human neural organoid models have become an important tool for studying neurobiology. In this work, we compared Matrigel to an N-cadherin peptide-functionalized gelatin methacryloyl hydrogel (termed GelMA-Cad) for culturing cortical neural organoids. Specifically, we compare five materials: (1) Matrigel, (2) GelMA-Cad with high crosslinker (HC), (3) GelMA-Cad with low crosslinker (LC), (4) GelMA HC and (5) GelMA LC. We determined that both mechanical properties and peptide presentation can tune cell fate and diversity in gelatin-based matrices during differentiation. Of particular note, cortical organoids cultured in GelMA-Cad produce higher numbers of neurogenic and ciliated radial glia and upper-layer excitatory neurons—an important population for modeling neurodegenerative disease—compared to GelMA and Matrigel controls.

2024-02-28 | E-MTAB-13828 | biostudies-arrayexpress

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