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RNA-seq of human and mouse stem-cell derived neurons and mouse primary cortical neurons after KCl-induced membrane depolarization against controls.

ABSTRACT: This experiment comprises RNA-seq data used to study evolutionary differences between humans and mice in neuronal activity-dependent transcriptional responses. Activity-dependent transcriptional responses in developing human stem cell-derived cortical neurons were compared with those induced in developing primary- or stem cell-derived mouse cortical neurons 4 hours after KCl-induced membrane depolarisation. Activity-dependent transcriptional responses were also measured in aneuploid mouse neurons carrying human chromosome 21, allowing study of the regulation of Hsa21 genes, plus their mouse orthologs, side-by-side in the same cellular environment of a mouse primary neuron.

ORGANISM(S): Mus musculus

PROVIDER: E-MTAB-5489 | BioStudies |

REPOSITORIES: biostudies

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RNA-seq of human and mouse stem-cell derived neurons and mouse primary cortical neurons after KCl-induced membrane depolarization against controls.

Project description:This experiment comprises RNA-seq data used to study evolutionary differences between humans and mice in neuronal activity-dependent transcriptional responses. Activity-dependent transcriptional responses in developing human stem cell-derived cortical neurons were compared with those induced in developing primary- or stem cell-derived mouse cortical neurons 4 hours after KCl-induced membrane depolarisation. Activity-dependent transcriptional responses were also measured in aneuploid mouse neurons carrying human chromosome 21, allowing study of the regulation of Hsa21 genes, plus their mouse orthologs, side-by-side in the same cellular environment of a mouse primary neuron.

2017-02-16 | E-MTAB-5489 | ArrayExpress

Global ubiquitylation analysis of mitochondria in primary neurons identifies endogenous Parkin targets following activation of PINK1

Project description:Mutations in PINK1 and Parkin lead to Parkinson’s disease. Cell culture-based studies have demonstrated that mitochondrial depolarisation induced by chemical uncouplers can activate PINK1 and Parkin activity. Very little is known on mitochondrial depolarisation signalling in post-mitotic neurons. We have established a primary mouse cortical neuron system to investigate mitochondrial depolarisation induced changes in the proteome. We have undertaken proteomic copy-number analysis to characterise the expression levels of all known Parkinson’s proteins in cortical neurons. We have also identified proteins whose expression is up-regulated or down-regulated following mitochondrial depolarisation.

2021-09-15 | PXD027614 | Pride

Transcription profiling of mouse KCl depolarization-regulated genes in cortical neurons

Project description:we used DNA microarray analysis to identify genes that are induced by neuronal activity in excitatory neurons at the time when inhibitory synapses are forming and maturing on them. Experiment Overall Design: We cultured cortical neurons for 7 DIV until the process of inhibitory synapse development was underway, and then depolarized the neurons with 50 mM of KCl to activate L-type voltage-sensitive calcium channels (L-VSCCs) for 0, 1 or 6 hours, the cells were lysed, mRNA isolated and hybridized to Affymetrix arrays. Data were collected from 3 independent experiments.

| E-GEOD-11256 | BioStudies

Genome-wide analysis of Gtf3c1, RNAP3 occupancy and H3K4me1, H3K27ac chromatin modifications in primary mouse cortical neurons

Project description:SINEs are a highly abundant class of retrotransposons that were initially considered a non-functional “junk” DNA due to their non coding, repetitive nature. SINEs frequently possess an internal RNAPIII promoter, which recruits the RNAPIII transcriptional machinery, including the general nuclear complex TFIIIC. We recently discovered that in response to neuronal depolarisation, SINEs may represent a novel class of neuronal enhancers and reasoned that RNAPIII and TFIIIC binding may provide a means of identifying enhancer SINEs genome-wide. To this end, we first performed ChIPseq analysis on resting and depolarised mouse cortical neurons, using an antibody that targets the DNA binding subunit of TFIIIC (Gtf3c1), RNA Polymerase III and the enhancer markers H3K4me1 and H3K27ac . Overall design: ChIPseq analysis of Gtf3c1, RNAP3, H3K4me1 and H3K27ac in primary mouse cortical neurons either untreated or depolarized with 50 mM KCl for 45 min. Total chromatin input was used as a control. For each experimental condition, 3 biological replicates were used.

2017-12-05 | GSE75191 | GEO

Evidence for evolutionary divergence of activity-dependent gene expression in developing neurons.

Project description:Evolutionary differences in gene regulation between humans and lower mammalian experimental systems are incompletely understood, a potential translational obstacle that is challenging to surmount in neurons, where primary tissue availability is poor. Rodent-based studies show that activity-dependent transcriptional programs mediate myriad functions in neuronal development, but the extent of their conservation in human neurons is unknown. We compared activity-dependent transcriptional responses in developing human stem cell-derived cortical neurons with those induced in developing primary- or stem cell-derived mouse cortical neurons. While activity-dependent gene-responsiveness showed little dependence on developmental stage or origin (primary tissue vs. stem cell), notable species-dependent differences were observed. Moreover, differential species-specific gene ortholog regulation was recapitulated in aneuploid mouse neurons carrying human chromosome-21, implicating promoter/enhancer sequence divergence as a factor, including human-specific activity-responsive AP-1 sites. These findings support the use of human neuronal systems for probing transcriptional responses to physiological stimuli or indeed pharmaceutical agents.

| S-EPMC5092045 | BioStudies

KCl depolarization-regulated genes in mouse cortical neurons

Project description:we used DNA microarray analysis to identify genes that are induced by neuronal activity in excitatory neurons at the time when inhibitory synapses are forming and maturing on them. Keywords: Primary neuron culture, depolarization, activity-dependent Overall design: We cultured cortical neurons for 7 DIV until the process of inhibitory synapse development was underway, and then depolarized the neurons with 50 mM of KCl to activate L-type voltage-sensitive calcium channels (L-VSCCs) for 0, 1 or 6 hours, the cells were lysed, mRNA isolated and hybridized to Affymetrix arrays. Data were collected from 3 independent experiments.

2008-09-24 | GSE11256 | GEO

Deficits in human trisomy 21 iPSCs and neurons.

Project description:Down syndrome (trisomy 21) is the most common genetic cause of intellectual disability, but the precise molecular mechanisms underlying impaired cognition remain unclear. Elucidation of these mechanisms has been hindered by the lack of a model system that contains full trisomy of chromosome 21 (Ts21) in a human genome that enables normal gene regulation. To overcome this limitation, we created Ts21-induced pluripotent stem cells (iPSCs) from two sets of Ts21 human fibroblasts. One of the fibroblast lines had low level mosaicism for Ts21 and yielded Ts21 iPSCs and an isogenic control that is disomic for human chromosome 21 (HSA21). Differentiation of all Ts21 iPSCs yielded similar numbers of neurons expressing markers characteristic of dorsal forebrain neurons that were functionally similar to controls. Expression profiling of Ts21 iPSCs and their neuronal derivatives revealed changes in HSA21 genes consistent with the presence of 50% more genetic material as well as changes in non-HSA21 genes that suggested compensatory responses to oxidative stress. Ts21 neurons displayed reduced synaptic activity, affecting excitatory and inhibitory synapses equally. Thus, Ts21 iPSCs and neurons display unique developmental defects that are consistent with cognitive deficits in individuals with Down syndrome and may enable discovery of the underlying causes of and treatments for this disorder.

| S-EPMC3683748 | BioStudies

Mouse models of Down syndrome: gene content and consequences.

Project description:Down syndrome (DS), trisomy of human chromosome 21 (Hsa21), is challenging to model in mice. Not only is it a contiguous gene syndrome spanning 35 Mb of the long arm of Hsa21, but orthologs of Hsa21 genes map to segments of three mouse chromosomes, Mmu16, Mmu17, and Mmu10. The Ts65Dn was the first viable segmental trisomy mouse model for DS; it is a partial trisomy currently popular in preclinical evaluations of drugs for cognition in DS. Limitations of the Ts65Dn are as follows: (i) it is trisomic for 125 human protein-coding orthologs, but only 90 of these are Hsa21 orthologs and (ii) it lacks trisomy for ~75 Hsa21 orthologs. In recent years, several additional mouse models of DS have been generated, each trisomic for a different subset of Hsa21 genes or their orthologs. To best exploit these models and interpret the results obtained with them, prior to proposing clinical trials, an understanding of their trisomic gene content, relative to full trisomy 21, is necessary. Here we first review the functional information on Hsa21 protein-coding genes and the more recent annotation of a large number of functional RNA genes. We then discuss the conservation and genomic distribution of Hsa21 orthologs in the mouse genome and the distribution of mouse-specific genes. Lastly, we consider the strengths and weaknesses of mouse models of DS based on the number and nature of the Hsa21 orthologs that are, and are not, trisomic in each, and discuss their validity for use in preclinical evaluations of drug responses.

| S-EPMC5471624 | BioStudies

Transcription profiling of mouse KCl depolarization-regulated genes in cortical neurons

2008-10-26 | E-GEOD-11256 | ArrayExpress

Nuclear Reorganization in Hippocampal Granule Cell Neurons from a Mouse Model of Down Syndrome: Changes in Chromatin Configuration, Nucleoli and Cajal Bodies.

Project description:Down syndrome (DS) or trisomy of chromosome 21 (Hsa21) is characterized by impaired hippocampal-dependent learning and memory. These alterations are due to defective neurogenesis and to neuromorphological and functional anomalies of numerous neuronal populations, including hippocampal granular cells (GCs). It has been proposed that the additional gene dose in trisomic cells induces modifications in nuclear compartments and on the chromatin landscape, which could contribute to some DS phenotypes. The Ts65Dn (TS) mouse model of DS carries a triplication of 92 genes orthologous to those found in Hsa21, and shares many phenotypes with DS individuals, including cognitive and neuromorphological alterations. Considering its essential role in hippocampal memory formation, we investigated whether the triplication of this set of Hsa21 orthologous genes in TS mice modifies the nuclear architecture of their GCs. Our results show that the TS mouse presents alterations in the nuclear architecture of its GCs, affecting nuclear compartments involved in transcription and pre-rRNA and pre-mRNA processing. In particular, the GCs of the TS mouse show alterations in the nucleolar fusion pattern and the molecular assembly of Cajal bodies (CBs). Furthermore, hippocampal GCs of TS mice present an epigenetic dysregulation of chromatin that results in an increased heterochromatinization and reduced global transcriptional activity. These nuclear alterations could play an important role in the neuromorphological and/or functional alterations of the hippocampal GCs implicated in the cognitive dysfunction characteristic of TS mice.

| S-EPMC7865916 | BioStudies

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