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Expression data from induced parvalbumin neurons.

ABSTRACT: Parvalbumin neurons, as an important subtype of inhibitory neurons, play a crucial role in the brain. The dysfunctions of those cells are associated with multiple neural system disorders. We carried out whole gene expression studies for the induction process of parvalbumin neurons. We used microarrays to detail the global program of gene expression underlying cellularization and identified distinct classes of up-regulated genes during this process. Induced parvalbumin neuron cells were selected at successive stages of induction process for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain homogeneous populations of induced parvalbumin neurons at each developmental stage in order to increase the temporal resolution of expression profiles.

ORGANISM(S): Mus musculus

SUBMITTER: Jianwei Jiao

PROVIDER: E-GEOD-79146 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from induced parvalbumin neurons.

Project description:Parvalbumin neurons, as an important subtype of inhibitory neurons, play a crucial role in the brain. The dysfunctions of those cells are associated with multiple neural system disorders. We carried out whole gene expression studies for the induction process of parvalbumin neurons. We used microarrays to detail the global program of gene expression underlying cellularization and identified distinct classes of up-regulated genes during this process.

2016-03-12 | GSE79146 | GEO

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Whole brain transcriptomic analysis of Tbr1-K228E mutant mice

Project description:Mutations of Tbr1, a high-confidence ASD (autism spectrum disorder)-risk gene encoding the transcription regulator TBR1, in mice have been shown to induce diverse ASD-related molecular, synaptic, neuronal, and behavioral dysfunctions. However, it remains unclear whether Tbr1 mutations derived from autistic individuals cause similar dysfunctions in mice remains unclear. Here we generated and characterized mice carrying the TBR1-K228E de novo mutation identified in human ASD and identified various ASD-related phenotypes. In heterozygous mice carrying this mutation (Tbr1+/K228E mice), the levels of the TBR1-K228E protein, which cannot bind to target DNA, were strongly increased. RNA-Seq analysis of the Tbr1+/K228E embryonic brain indicated significant changes in the expression of genes associated with neurons, astrocytes, ribosomes, neuronal synapses, and ASD risk. The Tbr1+/K228E neocortex displayed abnormal distribution of parvalbumin-positive interneurons, with the density lower in superficial layers but higher in deep layers. This was associated with increased inhibitory synaptic transmission in layer 6 pyramidal neurons, which was resistant to compensation by network activity. Behaviorally, Tbr1+/K228E mice showed decreased social interaction, increased self-grooming, and modestly increased anxiety-like behaviors. These results suggest that the human heterozygous TBR1-K228E mutation induces ASD-related protein, transcriptomic, neuronal, synaptic, and behavioral dysfunctions in mice.

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Mus musculus

Project description:Expression data from induced parvalbumin neurons.

| PRJNA315015 | ENA

Transcription profiling of human spinal muscular atrophy patient induced pluripotent stem cells

Project description:Spinal muscular atrophy (SMA) is one of the most common inherited forms of neurological disease leading to infant mortality. Patients exhibit selective loss of lower motor neurons resulting in muscle weakness, paralysis, and often death. Although patient fibroblasts have been used extensively to study SMA, motor neurons have a unique anatomy and physiology which may underlie their vulnerability to the disease process. Here we report the generation of induced pluripotent stem (iPS) cells from skin fibroblast samples taken from a child with SMA. These cells expanded robustly in culture, maintained the disease genotype, and generated motor neurons that showed selective deficits compared to those derived from the childâs unaffected mother. This is the first study to show human iPS cells can be used to model the specific pathology seen in a genetically inherited disease. As such, it represents a promising resource to study disease mechanisms, screen novel drug compounds, and develop new therapies. Experiment Overall Design: A total of 10 samples were hybridized to the human genome U133 Plus 2.0 GeneChip arrays carrying 54,675 probe sets (Affimetrix). Experiment Overall Design: H1L, H7, H9, H13B, and H14A embryonic stem cells are controls for the iPS cells Experiment Overall Design: iPS(SMA) 3.5 and iPS(SMA)3.6 are from the patient. The clone iPS(SMA) 4.2. is from the parent.

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Gene expression from human fibroblasts

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