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Bulk transcriptome analysis of conditional MYT1L-mutant ESC-derived human induced neurons.

ABSTRACT: Bulk transcriptome analysis of conditional MYT1L-mutant ESC-derived human induced neurons.

PROVIDER: PRJNA719236 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14130300_1.fastq.gz	Fastqsanger.gz
	SRR14130300_2.fastq.gz	Fastqsanger.gz
	SRR14130301_1.fastq.gz	Fastqsanger.gz
	SRR14130301_2.fastq.gz	Fastqsanger.gz
	SRR14130302_1.fastq.gz	Fastqsanger.gz

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Bulk transcriptome analysis of conditional MYT1L-mutant ESC-derived human induced neurons.

Project description:We examined the effect of heterozygous MYT1L deficiency in human induced neurons. Increased expression of genes with MYT1L binding motifs and activation of non-neuronal genes were observed in human neurons along with deregulation of autism-associated risk genes upon depletion of MYT1L.

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Bulk transcriptome analysis of conditional MYT1L-mutant ESC-derived human induced neurons following Wnt and/or Notch inhibitor treatment.

Project description:We examined the effect of Wnt and/or Notch inhibition in the context of heterozygous MYT1L deficiency in human induced neurons. Increased expression of genes with MYT1L binding motifs and activation of non-neuronal genes were observed in human neurons along with deregulation of autism-associated risk genes upon depletion of MYT1L.

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Project description:Bulk transcriptome analysis of conditional MYT1L-mutant ESC-derived human induced neurons following Wnt and/or Notch inhibitor treatment.

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MYT1L haploinsufficiency in human neurons and mice causes autism-associated phenotypes that can be reversed by genetic and pharmacologic intervention

Project description:MYT1L is an autism spectrum disorder (ASD)-associated transcription factor that is expressed in virtually all neurons throughout life. How MYT1L mutations cause neurological phenotypes and whether they can be targeted remains enigmatic. Here, we examine the effects of MYT1L deficiency in human neurons and mice. Mutant mice exhibit neurodevelopmental delays with thinner cortices, behavioural phenotypes, and gene expression changes that resemble those of ASD patients. MYT1L target genes, including WNT and NOTCH, are activated upon MYT1L depletion and their chemical inhibition can rescue delayed neurogenesis in vitro. MYT1L deficiency also causes upregulation of the main cardiac sodium channel, SCN5A, and neuronal hyperactivity, which could be restored by shRNA-mediated knockdown of SCN5A or MYT1L overexpression in postmitotic neurons. Acute application of the sodium channel blocker, lamotrigine, also rescued electrophysiologic defects in vitro and behaviour phenotypes in vivo. Hence, MYT1L mutation causes both developmental and postmitotic neurological defects. However, acute intervention can normalise resulting electrophysiological and behavioural phenotypes in adulthood.

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Bulk transcriptome analysis of Myt1l mutant mouse neuron primary cultures.

Project description:We examined the effect of Myt1l deficiency in the neurons of mice. Homozygous Myt1l deficiency resulted in postnatal lethality, and mutant mice presented gene expression changes associated with developmental delays and resembled changes observed in autism spectrum disorder patients.

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

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