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Differences and similarities between human and chimpanzee neural progenitors during cerebral cortex development

ABSTRACT: Differences and similarities between human and chimpanzee neural progenitors during cerebral cortex development

OTHER RELATED OMICS DATASETS IN: GSE86207

PROVIDER: PRJNA340888 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR4095720_1.fastq.gz	Fastqsanger.gz
	SRR4095720_2.fastq.gz	Fastqsanger.gz
	SRR4095730_1.fastq.gz	Fastqsanger.gz
	SRR4095730_2.fastq.gz	Fastqsanger.gz
	SRR4095740_1.fastq.gz	Fastqsanger.gz

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Differences and similarities between human and chimpanzee neural progenitors during cerebral cortex development.

Project description:Human neocortex expansion likely contributed to the remarkable cognitive abilities of humans. This expansion is thought to primarily reflect differences in proliferation versus differentiation of neural progenitors during cortical development. Here, we have searched for such differences by analysing cerebral organoids from human and chimpanzees using immunohistofluorescence, live imaging, and single-cell transcriptomics. We find that the cytoarchitecture, cell type composition, and neurogenic gene expression programs of humans and chimpanzees are remarkably similar. Notably, however, live imaging of apical progenitor mitosis uncovered a lengthening of prometaphase-metaphase in humans compared to chimpanzees that is specific to proliferating progenitors and not observed in non-neural cells. Consistent with this, the small set of genes more highly expressed in human apical progenitors points to increased proliferative capacity, and the proportion of neurogenic basal progenitors is lower in humans. These subtle differences in cortical progenitors between humans and chimpanzees may have consequences for human neocortex evolution.

| S-EPMC5110243 | biostudies-literature

Differences and similarities between human and chimpanzee neural progenitors during cerebral cortex development

Project description:Human neocortex expansion likely contributed to the remarkable cognitive abilities of humans. This expansion is thought to primarily reflect differences in proliferation versus differentiation of neural progenitors during cortical development. Here, we have searched for such differences by analysing cerebral organoids from human and chimpanzees using immunohistochemistry, live imaging, and single-cell transcriptomics. We find that the cytoarchitecture, cell type composition, and neurogenic gene expression programs of humans and chimpanzees are remarkably similar. Notably, however, live imaging of apical progenitor mitosis uncovered a lengthening of prometaphase-metaphase in humans compared to chimpanzees that is specific to proliferating progenitors and not observed in non-neural cells. Consistent with this, the small set of genes more highly expressed in human apical progenitors points to increased proliferative capacity, and the proportion of neurogenic basal progenitors is lower in humans. These subtle differences in cortical progenitors between humans and chimpanzees may have consequences for human neocortex evolution.

2016-11-04 | GSE86207 | GEO

Single-cell ATAC-seq of chimpanzee cerebral organoids

Project description:Single cell ATAC-seq (scATAC-seq) was performed at various stages of differentiation of chimpanzee induced pluripotent stem cells (iPSC) to 4 month old cerebral organoids. scATAC-seq was performed on the following days of differentiation: day 0 (pluripotent stem cell), day 4 (embryoid body), day 10 (neuroectoderm), day 15 (neuroepithelium), day 30 (1 month old cerebral organoid), day 60 (2 months old cerebral organoid), and day 120 (4 months old cerebral organoid).

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Expression data from mouse cerebral cortex

Project description:Differential gene expression of cerebral cortex might be responsible for distinct neurovascular developments between different mouse strains We used Affymetrix microarray to explore the global gene expression patterns of mouse cerebral cortex of different mouse strains at two developmental stages Cerebral cortex from two mouse strains [C57BL/6J(B6) and C3H/J (C3H)] at post-natal day 1 (p1) and post-natal 11 weeks (11 wk) were harvested for microarray experiments

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Project description:Pluripotent stem cells (PSC) can differentiate inot any cell type of an organism. Their remarkable capability of self-organization enables the formation of three-dimensional structures that resembles miniature organs, including cerebral organoids. These organoids can recreate early steps of the human cerebral cortex development, and show great potential for modeling human diseases, particularly for those with a developmental component. This data evidences stem cell-derived cerebral organoids as a key model to study brain development and neurodevelopmental, neurodegenerative and neuropsychiatric diseases.

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Single-cell ATAC-seq of chimpanzee cerebral organoids

Project description:Single-cell ATAC-seq of chimpanzee cerebral organoids

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Expression data from mouse cerebral cortex

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Project description:BACKGROUND: The protozoan parasite Toxoplasma gondii infects and alters the neurotransmission in cerebral cortex and other brain regions, leading to neurobehavioral and neuropathologic changes in humans and animals. However, the molecules that contribute to these changes remain largely unknown.METHODS: We have investigated the impact of T. gondii infection on the overall metabolism of mouse cerebral cortex. Mass-spectrometry-based metabolomics and multivariate statistical analysis were employed to discover metabolomic signatures that discriminate between cerebral cortex of T. gondii-infected and uninfected control mice.RESULTS: Our results identified 73, 67 and 276 differentially abundant metabolites, which were involved in 25, 37 and 64 pathways at 7, 14 and 21 days post-infection (dpi), respectively. Metabolites in the unsaturated fatty acid biosynthesis pathway were upregulated as the infection progressed, indicating that T. gondii induces the biosynthesis of unsaturated fatty acids to promote its own growth and survival. Some of the downregulated metabolites were related to pathways, such as steroid hormone biosynthesis and arachidonic acid metabolism. Nine metabolites were identified as T. gondii responsive metabolites, namely galactosylsphingosine, arachidonic acid, LysoSM(d18:1), L-palmitoylcarnitine, calcitetrol, 27-Deoxy-5b-cyprinol, L-homophenylalanine, oleic acid and ceramide (d18:1/16:0).CONCLUSIONS: Our data provide novel insight into the dysregulation of the metabolism of the mouse cerebral cortex during T. gondii infection and have important implications for studies of T. gondii pathogenesis.

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Sex Differences in the Neuronal Transcriptome and Synaptic Mitochondrial Function in Cerebral Cortex of a Multiple Sclerosis Model

Project description:Multiple sclerosis (MS) affects the cerebral cortex, inducing cortical atrophy and neuronal and synaptic pathology. Despite the fact that women are more susceptible to getting MS, men with MS have worse disability progression. Here, we address sex differences in neurodegenerative mechanisms focusing on the cerebral cortex using the MS model, chronic experimental autoimmune encephalomyelitis (EAE). RNA sequencing of neurons in cerebral cortex during EAE showed robust differential gene expression in male EAE mice compared to male healthy, age-matched, control mice. In contrast, there were few differences in female EAE mice compared to female controls. The most enriched differential gene expression pathways in male mice during EAE were mitochondrial dysfunction and oxidative phosphorylation. Mitochondrial morphology showed significant abnormalities in the cerebral cortex of EAE males, but not EAE females. Regarding function, synaptosomes isolated from cerebral cortex of male EAE mice demonstrated decreased oxygen consumption rates during respirometry assays. Together, cortical neuronal transcriptomics, mitochondrial morphology, and functional respirometry assays in synaptosomes revealed worse neurodegeneration in male EAE mice. This is consistent with worse neurodegeneration in MS men and reveals a model and a target to develop treatments to prevent cortical neurodegeneration and mitigate disability progression in MS men.

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Human and Rhesus macaque cerebral cortex DNA methylation by MeDIP-Chip

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