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Regulatory elements with preferential activity in cortical interneurons identified by histone modification ChIP-seq

ABSTRACT: Regulatory elements with preferential activity in cortical interneurons identified by histone modification ChIP-seq

PROVIDER: PRJNA665215 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12697628.fastq.gz	Fastqsanger.gz
	SRR12697629.fastq.gz	Fastqsanger.gz
	SRR12697630.fastq.gz	Fastqsanger.gz
	SRR12697631.fastq.gz	Fastqsanger.gz
	SRR12697632.fastq.gz	Fastqsanger.gz

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Regulatory elements with preferential activity in cortical interneurons identified by histone modification ChIP-seq

2020-09-24 | GSE158428 | GEO

Rbfox1 mediates cell-type specific splicing in cortical interneurons

Project description:Cortical interneurons display a remarkable diversity in their morphology, physiological properties and connectivity. Elucidating the molecular determinants underlying this heterogeneity is essential for understanding interneuron development and function. We discovered that alternative splicing differentially regulates the integration of somatostatin- and parvalbumin-expressing interneurons into nascent cortical circuits through the cell-type specific tailoring of mRNAs. Specifically, we identified a role for the activity-dependent splicing regulator Rbfox1 in the development of cortical interneuron subtype specific efferent connectivity. Our work demonstrates that Rbfox1 mediates largely non-overlapping alternative splicing programs within two distinct but related classes of interneurons.

2018-10-12 | GSE119998 | GEO

Developmental diversification of cortical inhibitory interneurons

Project description:Developmental diversification of cortical inhibitory interneurons

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DOT1L deletion impairs the development of cortical Parvalbumin-expressing interneurons

Project description:Our group has reported that the histone methyltransferase DOT1L is necessary for proper cortical plate development and layer distribution of glutamatergic neurons, however, its specific role on cortical interneuron development has not yet been explored. Here, we demonstrate that DOT1L affects interneuron development in a cell-autonomous manner. Deletion of Dot1l in MGE-derived interneuron precursor cells results in an overall reduction and altered distribution of GABAergic interneurons in the cortical plate at postnatal day (P) 0. Furthermore, we observed an altered proportion of GABAergic interneurons in the cortex and striatum at P21 with a significant decrease in Parvalbumin (PVALB)-expressing interneurons. Altogether, our results indicate that reduced numbers of cortical interneurons upon DOT1L deletion results from altered postmitotic differentiation/maturation.

2023-08-01 | GSE221994 | GEO

Single-cell RNA-seq of developing cortical interneurons

Project description:Single-cell RNA-sequencing of cortical GABAergic interneurons to characterize their transcriptional profiles at several timepoints across development - from their origins in the ganglionic eminences, upon migration to the cortex, settling in cortical laminae, and through maturation.

2021-09-22 | GSE164570 | GEO

Single-cell ATAC-seq of developing cortical interneurons.

Project description:Single-cell ATAC-sequencing of cortical GABAergic interneurons to characterize the chromatin landscapes of these cells at several timepoints across development - from their origins in the ganglionic eminences, upon migration to the cortex, settling in cortical laminae, and through maturation.

2021-09-22 | GSE165031 | GEO

ChIP-seq profile of iPSC-derived human developmental cortical interneurons

Project description:ChIP-seq was carried out by high throughput sequencing in human developmental cortical interneurons derived from healthy control vs schizophrenia iPSCs

2022-12-31 | GSE186738 | GEO

Regulatory Elements Inserted into AAVs Confer Preferential Activity in Cortical Interneurons.

Project description:Cortical interneuron (CIN) dysfunction is thought to play a major role in neuropsychiatric conditions like epilepsy, schizophrenia and autism. It is therefore essential to understand how the development, physiology, and functions of CINs influence cortical circuit activity and behavior in model organisms such as mice and primates. While transgenic driver lines are powerful tools for studying CINs in mice, this technology is limited in other species. An alternative approach is to use viral vectors such as AAV, which can be used in multiple species including primates and also have potential for therapeutic use in humans. Thus, we sought to discover gene regulatory enhancer elements (REs) that can be used in viral vectors to drive expression in specific cell types. The present study describes the systematic genome-wide identification of putative REs (pREs) that are preferentially active in immature CINs by histone modification chromatin immunoprecipitation and sequencing (ChIP-seq). We evaluated two novel pREs in AAV vectors, alongside the well-established Dlx I12b enhancer, and found that they drove CIN-specific reporter expression in adult mice. We also showed that the identified Arl4d pRE could drive sufficient expression of channelrhodopsin for optogenetic rescue of behavioral deficits in the Dlx5/6 +/- mouse model of fast-spiking CIN dysfunction.

| S-EPMC7768279 | biostudies-literature

Genome-wide transcriptome analysis of human iPSC-derived migratory cortical interneurons.

Project description:We report changes of gene expression in migratory cortical interneurons derived from healthy control vs schizophrenia iPSCs by genome-wide transcriptome analysis.

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PlexinA4-Semaphorin3A mediated crosstalk between main cortical interneuron classes is required for superficial interneurons lamination

Project description:In the mammalian cerebral cortex, the developmental events governing the allocation of different classes of inhibitory neurons into distinct cortical layers are poorly understood. Here we report that the guidance receptor PlexinA4 is upregulated in serotonin receptor 3a-expressing (HTR3A) cortical interneurons (hINs) as they invade the cortical plate and that it regulates their laminar allocation to superficial cortical layers. We find that the PlexinA4 ligand Semaphorin3A acts as a chemorepulsive factor on hINs migrating into the nascent cortex and demonstrate that Semaphorin3A specifically controls their laminar positioning through PlexinA4. We identify that deep layer interneurons constitute a major source of Semaphorin3A in the developing cortex and demonstrate that cell-type specific genetic deletion of Semaphorin3A in these interneurons specifically affects the laminar allocation of hINs. These data demonstrate that in the neocortex, deep layer interneurons control the laminar allocation of hINs into superficial layers.

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