Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-cell transcriptome analysis of Myt1l mutant mouse cortices at birth.

ABSTRACT: We examined the effect of Myt1l deficiency in the cortices of mice at birth on the single cell level. Homozygous Myt1l deficiency resulted in postnatal lethality, and mutant mice presented increased expression of non-neuronal genes in neurons.

ORGANISM(S): Mus musculus

PROVIDER: GSE171326 | GEO | 2023/02/14

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	GSE171326_mouse_single_cell_MAST_meld_het_vs_wt.tsv.gz	Tabular
	GSE171326_mouse_single_cell_MAST_meld_hom_vs_wt.tsv.gz	Tabular
	GSE171326_mouse_single_cell_metadata.tsv.gz	Tabular
	GSE171326_mouse_single_cell_raw_cell_x_gene.tsv.gz	Tabular

Items per page:

1 - 5 of 5

Similar Datasets

Bulk transcriptome analysis of Myt1l mutant mouse cortices across development.

Project description:We examined the effect of Myt1l deficiency in the cortices of mice during developement. 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.

2023-02-14 | GSE171325 | GEO

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.

2023-02-14 | GSE217554 | GEO

Single-cell transcriptome analysis of Myt1l mutant mouse cortices at birth.

Project description:Single-cell transcriptome analysis of Myt1l mutant mouse cortices at birth.

| PRJNA719238 | ENA

CUT&RUN analysis of MYT1L binding in mouse cortices across development.

Project description:We examined MYT1L binding in the genome within cortices of mice during developement.

2023-02-14 | GSE217553 | GEO

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.

2023-02-20 | PXD037867 | Pride

Bulk transcriptome analysis of Myt1l mutant mouse cortices across development.

Project description:Bulk transcriptome analysis of Myt1l mutant mouse cortices across development.

| PRJNA719237 | ENA

CUT&RUN analysis of MYT1L binding in mouse cortices across development.

Project description:CUT&RUN analysis of MYT1L binding in mouse cortices across development.

| PRJNA899526 | ENA

MYT1L-deficiency and brain

Project description:MYT1L-deficiency and brain

| PRJNA719125 | ENA

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 [E14]

2024-04-11 | GSE262364 | GEO