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MYT1L loss leads to chromatin structures and transcriptome alterations in mouse hypothalamus [RNA-Seq]

ABSTRACT: MYT1L Syndrome mouse model displays obesity as observed in MYT1L patients. Utilizing this mouse model, ATAC-seq and RNA-seq on adult mouse hypothalamus reveals molecular alternations related to feeding behaviors, which might contribute to obesity phenotype.

ORGANISM(S): Mus musculus

PROVIDER: GSE173922 | GEO | 2024/12/18

REPOSITORIES: GEO

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MYT1L loss leads to chromatin structures and transcriptome alterations in mouse hypothalamus [ATAC-Seq]

Project description:MYT1L Syndrome mouse model displays obesity as observed in MYT1L patients. Utilizing this mouse model, ATAC-seq and RNA-seq on adult mouse hypothalamus reveals molecular alternations related to feeding behaviors, which might contribute to obesity phenotype.

2024-12-18 | GSE173585 | GEO

MYT1L loss leads to chromatin structures and transcriptome alterations in mouse hypothalamus

Project description:MYT1L loss leads to chromatin structures and transcriptome alterations in mouse hypothalamus

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MYT1L loss leads to chromatin structures and transcriptome alterations in mouse hypothalamus [ATAC-Seq]

Project description:MYT1L loss leads to chromatin structures and transcriptome alterations in mouse hypothalamus [ATAC-Seq]

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MYT1L loss leads to chromatin structures and transcriptome alterations in mouse hypothalamus [RNA-Seq]

Project description:MYT1L loss leads to chromatin structures and transcriptome alterations in mouse hypothalamus [RNA-Seq]

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MYT1L loss leads to chromatin structures and transcriptome alterations in mouse hypothalamus

Project description:This SuperSeries is composed of the SubSeries listed below.

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Hypothalamus proteomics from mouse models with obesity and anorexia reveals novel therapeutic targets of appetite regulation

Project description:This study examined the proteomic profile of hypothalamus in mouse models of obesity and anorexia

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A MYT1L Syndrome mouse model recapitulates patient phenotypes and reveals altered brain development due to disrupted neuronal maturation [RNA-Seq]

Project description:Human genetics have defined a new autism-associated syndrome caused by loss-of-function mutations in MYT1L, a transcription factor known for enabling fibroblast-to-neuron conversions. However, how MYT1L mutation causes autism, ADHD, intellectual disability, obesity, and brain anomalies is unknown. Here, we develop a mouse model of this syndrome. Physically, Myt1l haploinsufficiency causes obesity, white-matter thinning, and microcephaly in the mice, mimicking clinical phenotypes. Studies during brain development reveal disrupted gene expression, mediated in part by loss of Myt1l gene target activation, and highlight precocious neuronal differentiation as the mechanism for microcephaly. In contrast, adult studies reveal that mutation results in failure of transcriptional and chromatin maturation, echoed in disruptions in baseline physiological properties of neurons. This results in behavioral features including hyperactivity, hypotonia, and social alterations, with more severe phenotypes in males. Overall, these studies provide insight into the mechanistic underpinnings of this disorder and enable future preclinical studies.

2021-09-22 | GSE173926 | GEO

A MYT1L Syndrome mouse model recapitulates patient phenotypes and reveals altered brain development due to disrupted neuronal maturation [ATAC-Seq]

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Profiling of hypothalamus tissue from the F2 M16xICR mouse cross.

Project description:We profiled gene expression in hypothalamus tissue from F2 progeny from a cross between the outbred M16 (selectively bred for rapid weight gain) and ICR (control) mouse strains. We developed a framework for reconstructing tissue-to-tissue coexpression networks between genes in hypothalamus, liver or hypothalamus tissues that are independent of networks constructed from single tissue analyses. The subnetworks we identify as specific to tissue-to-tissue interactions associate with multiple obesity-relevant biological functions like circadian rhythm, energy balance, stress response, or immune response. Keywords: Tissue profiling in a mouse F2 cross. We analyzed 308 hypothalamus samples.

2010-06-22 | E-GEOD-13745 | biostudies-arrayexpress

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

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