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Brain transcriptome analysis of Myt1l heterozygote mutation mice in different brain regions (RNA-Seq II)

ABSTRACT: Brain transcriptome analysis of Myt1l heterozygote mutation mice in different brain regions (RNA-Seq II)

PROVIDER: PRJNA851808 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19786538_1.fastq.gz	Fastqsanger.gz
	SRR19786538_2.fastq.gz	Fastqsanger.gz
	SRR19786539_1.fastq.gz	Fastqsanger.gz
	SRR19786539_2.fastq.gz	Fastqsanger.gz
	SRR19786540_1.fastq.gz	Fastqsanger.gz

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Brain transcriptome analysis of Myt1l heterozygote mutation mice

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Brain transcriptome analysis of Myt1l heterozygote mutation mice in different brain regions (RNA-Seq II)

Project description:Myt1l, a zinc-finger transcription factor, promotes neuronal differentiation and is implicated in autism spectrum disorders (ASD) and intellectual disability. However, it was previously unclear whether Myt1l promotes neuronal differentiation in vivo, how its deficiency leads to disease-related mouse phenotypes, and whether and how ASD-risk genes with strong embryonic and perinatal gene expression can yield strong adult-stage ASD-related phenotypes. Here, we report that Myt1l-heterozygous knockout (Myt1l-HT) mice display postnatal age-differential ASD-like phenotypes: Newborn Myt1l-HT mice show ASD-like transcriptomic changes involving suppressed neuronal and synaptic gene expression and suppressed right reflex. Juvenile Myt1l-HT mice display mixed ASD-like and reverse-ASD transcriptomic patterns and large normal behaviors, accompanying increased prefrontal excitatory synaptic transmission. However, adult Myt1l-HT mice show additional ASD-like transcriptomic changes involving astrocytic and microglial genes, along with behavioral deficits and excessive prefrontal inhibitory synaptic transmission. Therefore, Myt1l HT leads to newborn-stage ASD-like neuronal suppression, temporary juvenile normalization, and subsequent adult-stage ASD-like deficits.

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Brain transcriptome analysis of Myt1l heterozygote mutation mice (RNA-Seq I)

Project description:Myt1l is a transcription factor for neuronal induction and maintenance during development and Myt1l is highly implicated in autism spectrum disorder (ASD). Myt1l-mutant mice with a heterozygous deletion of exon 9 showed mild autistic-like behaviors (Social deficit and specific repetitive behaviors) and additional behavioral abnormalities including hyperactivity and anxiolytic-like behaviors in adult. To explore the molecular patterns and mechanisms underlying these behavioral abnormalities, we performed RNA-seq analysis of whole brain from wild-type and Myt1l-mutant mice longitudinally from pup stage (~P3) to juvenile (~P21) and adult (~P56) stages. Myt1l-mutant mice showed upregulations of chromosome- and chromatin-related genes and downregulations of synapse- and neurotransmitter-related genes during pup stage. However, from juvenile stage, Myt1l-mutant mice showed upregulations of extracellular matrix- and transporter-related genes and downregulations of mitochondria- and ribosome-related genes. In addition, Myt1l-mutant mice showed pro-ASD transcriptomic patterns on pup stage, but these patterns were reversed toward anti-ASD transcriptomic patterns from juvenile stages to adult stage as compensatory changes likely. These results suggest that the haploinsufficiency of Myt1l acutely alters the transcriptomic pattern into pro-ASD patterns and chronically compensates with the synapse maturation.

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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.

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

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Brain transcriptome analysis of Myt1l heterozygote mutation mice

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

2025-06-17 | GSE206718 | GEO

MYT1L is required for suppressing earlier neuronal development programs in the adult mouse brain

Project description:In vitro studies indicate the neurodevelopmental disorder gene Myelin Transcription Factor 1 Like (MYT1L) suppresses non-neuronal lineage genes during fibroblast-to-neuron direct differentiation. However, MYT1L’s molecular and cellular functions during differentiation in the mammalian brain have not been fully characterized. Here, we found that MYT1L loss leads to up-regulated deep layer (DL) but down-regulated upper layer (UL) neuron gene expression, corresponding to an increased ratio of DL/UL neurons in mouse cortex. To define potential mechanisms, we conducted Cleavage Under Targets & Release Using Nuclease (CUT&RUN) to map MYT1L binding targets in mouse developing cortex and adult prefrontal cortex (PFC), and to map epigenetic changes due to MYT1L mutation. We found MYT1L mainly binds to open chromatin, but with different transcription factor co-occupancies between promoters and enhancers. Likewise, multi-omic dataset integration revealed that, at promoters, MYT1L loss does not change chromatin accessibility but does increase H3K4me3 and H3K27ac, activating both a subset of earlier neuronal development genes as well as BCL11B, a key regulator for DL neuron development. Meanwhile, we discovered that MYT1L normally represses the activity of neurogenic enhancers associated with neuronal migration and neuronal projection development by closing chromatin structures and promoting removal of active histone marks. Further, we show MYT1L interacts with SIN3B and HDAC2 in vivo, providing potential mechanisms underlying any repressive effects on histone acetylation and gene expression. Overall, our findings provide a comprehensive map of MYT1L binding in vivo and mechanistic insights to how MYT1L facilitates neuronal maturation.

2023-03-02 | GSE222072 | GEO

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