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MYT1L genome-wide occupancy in human pluripotent stem cell-derived cortical interneurons

ABSTRACT: MYT1L genome-wide occupancy in human pluripotent stem cell-derived cortical interneurons

PROVIDER: PRJNA1021616 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26197757_1.fastq.gz	Fastqsanger.gz
	SRR26197757_2.fastq.gz	Fastqsanger.gz
	SRR26197758_1.fastq.gz	Fastqsanger.gz
	SRR26197758_2.fastq.gz	Fastqsanger.gz
	SRR26197759_1.fastq.gz	Fastqsanger.gz

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MYT1L genome-wide occupancy in human pluripotent stem cell-derived cortical interneurons

Project description:We have used our protocol for generating cortical interneurons from human pluripotent stem cells to study MYT1L genome-wide occupancy in human cortical interneurons.

2025-01-18 | GSE244185 | GEO

Transcriptomic analysis of ASD and IDD associated pathogenic MYT1L S707Q mutation in human cortical interneurons

Project description:We have used our protocol for generating cortical interneurons from human stem cells to study gene expression changes caused by the (S707QfsX56) mutation in the MYT1L gene, using both patient derived (PD) and variant knock in (VKI) models.

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MYT1L deficiency impairs excitatory neuron trajectory during cortical development [P1]

Project description:Mutations that reduce the function of MYT1L, a neuron-specific transcription factor, are associated with a syndromic neurodevelopmental disorder. Furthermore, MYT1L is routinely used as a pro-neural factor in fibroblast-to-neuron transdifferentiation. MYT1L has been hypothesized to play a role in the trajectory of neuronal specification and subtype specific maturation, but this hypothesis has not been directly tested, nor is it clear which neuron types are most impacted by MYT1L loss. In this study, we profiled 412,132 nuclei from the forebrains of wild-type and MYT1L-deficient mice at three developmental stages: E14 at the peak of neurogenesis, P1 when neurons in the six cortical layers have been born, and P21 when neurogenesis is complete and neurons are maturing, to examine the role of MYT1L levels in the trajectory of neuronal development. We found that MYT1L deficiency significantly disrupted the relative proportions of cortical excitatory neurons. Changes in gene expression were concentrated in excitatory neurons, suggesting that transcriptional effects of MYT1L deficiency are largely due to disruption of neuronal maturation programs. Most effects on gene expression were cell autonomous and persistent through development. In addition, while MYT1L can both activate and repress gene expression, the repressive effects were most sensitive to haploinsufficiency, and thus more likely mediate MYT1L syndrome. These findings illuminate the intricate role of MYT1L in orchestrating gene expression dynamics during neuronal development, providing insights into the molecular underpinnings of MYT1L syndrome.

2024-08-12 | GSE274102 | GEO

MYT1L deficiency impairs excitatory neuron trajectory during cortical development [P21]

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MYT1L deficiency impairs excitatory neuron trajectory during cortical development [E14]

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Transcriptomic analysis of ASD and IDD associated pathogenic MYT1L S707Q mutation in human cortical interneurons

Project description:Transcriptomic analysis of ASD and IDD associated pathogenic MYT1L S707Q mutation in human cortical interneurons

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Directed differentiation of human pluripotent stem cells into cortical interneurons

Project description:Here we demonstrate the highly efficient derivation of human cortical interneurons in a NKX2.1::GFP hESC reporter line. Manipulating the timing of SHH activation yields three distinct GFP+ populations with specific transcriptional profiles, neurotransmitter phenotypes and migratory behaviors. Total RNA was isolated at day 18 of differentiation from FACS sorted NKX2.1::GFP+ cells from three varying differentiation conditions and a “No SHH” condition (no sonic hedgehog treatment) that did not contain any GFP-expressing cells (Trizol, Sigma). Samples for each group in triplicate were processed for Illumina bead arrays (Illumina HT-12) by the MSKCC genomics core facility according to the specifications of the manufacturer.

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Project description:Disruption of parvalbumin positive (PVALB+) cortical interneurons is implicated in the pathogenesis of schizophrenia. However, how these defects emerge during development is not well understood. The protracted maturation of these cells during postnatal development has made their derivation from human pluripotent stem cells (hPSCs) extremely difficult, precluding hPSC-based disease modeling of their role in neuropsychiatric diseases. Here we present a cortical assembloid system that supports the development of PVALB+ cortical interneurons which match the molecular profiles of primary PVALB+ interneurons and display their distinctive electrophysiological features. Further, we characterized cortical interneuron development in a series of CRISPR-generated isogenic structural variants associated with schizophrenia and identified variant-specific phenotypes in cortical interneuron migration and the molecular profile of PVALB+ cortical interneurons. These findings reveal plausible mechanisms on how disruption of cortical interneuron development may impact schizophrenia risk and provide an exciting human experimental platform to facilitate the study of PVALB+ cortical interneurons.

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