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Brain methylome remodeling sustains neuronal activity gene expression in mice exposed to maternal immune activation [5mC]

ABSTRACT: Brain methylome remodeling sustains neuronal activity gene expression in mice exposed to maternal immune activation [5mC]

PROVIDER: PRJNA1003537 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25573550_1.fastq.gz	Fastqsanger.gz
	SRR25573550_2.fastq.gz	Fastqsanger.gz
	SRR25573551_1.fastq.gz	Fastqsanger.gz
	SRR25573551_2.fastq.gz	Fastqsanger.gz
	SRR25573552_1.fastq.gz	Fastqsanger.gz

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Brain methylome remodeling sustains neuronal activity gene expression in mice exposed to maternal immune activation [5mC]

Project description:Maternal infections have been linked to various neuropsychiatric disorders that may later emerge in offspring. 5-hydroxymethylcytosine (5hmC) and 5-methylcytosine (5mC) are key DNA modifications but their roles in maternal infection remain to be elucidated. It has been documented that Zika virus (ZIKV) infection during pregnancy leads to structural brain defects such as microcephaly in offspring. However, whether and how offspring exposed to maternal ZIKV infection develop neurocognitive complications remain largely unknown. Here we report that ZIKV infection during mouse pregnancy leads to offspring with depression- and anxiety-like behaviors, which are transmitted to the next generation. Single nucleus RNA sequencing in prefrontal cortex (PFC) of ZIKV offspring mice revealed cell type-specific gene dysregulation associated with neuropsychiatric lesions. Genome-wide 5hmC, 5mC, and transcriptome profiling in ZIKV PFC revealed an overall loss of 5hmC and an increase of 5mC in intragenic regions, associated with transcriptional changes in key functional genes. Gain-of-5hmC regions were mainly located in intergenic transposable elements (TEs) coupled with decreased 5mC and dynamic TE expression. These results provide the first 5hmC study in maternal infection and suggest that maternal ZIKV infection remodels methylome and gene expression in offspring mouse brains, contributing to transgenerational behavior changes.

2023-10-25 | GSE240413 | GEO

Brain methylome remodeling sustains neuronal activity gene expression in mice exposed to maternal immune activation [5hmc]

2023-10-25 | GSE240415 | GEO

Brain methylome remodeling sustains neuronal activity gene expression in mice exposed to maternal immune activation

Project description:Brain methylome remodeling sustains neuronal activity gene expression in mice exposed to maternal immune activation

| PRJNA1003534 | ENA

Brain methylome remodeling sustains neuronal activity gene expression in mice exposed to maternal immune activation [5hmc]

Project description:Brain methylome remodeling sustains neuronal activity gene expression in mice exposed to maternal immune activation [5hmc]

| PRJNA1003538 | ENA

Methylome of 5mC and 5hmC regulated by NEIL2

Project description:To elucidate the role of DNA glycosylase NEIL2 in regulation of DNA methylome, we performed genome sequencing of epigenetic marker 5mC and 5hmC in genome-wide using enyme-based library methods of TAPS and CAPS. The 5mC and 5hmC profile in CpG contect was further extracted and analysed.

2023-12-13 | GSE240177 | GEO

Brain methylome remodeling sustains neuronal activity gene expression in mice exposed to maternal immune activation

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

2023-10-25 | GSE240417 | GEO

Methylome of 5mC and 5hmC regulated by NEIL2

Project description:Methylome of 5mC and 5hmC regulated by NEIL2

| PRJNA1002410 | ENA

Brain methylome remodeling selectively regulates neuronal activity genes linking to emotional behaviors in mice exposed to maternal immune activation.

Project description:How early life experience is translated into storable epigenetic information leading to behavioral changes remains poorly understood. Here we found that Zika virus (ZIKV) induced-maternal immune activation (MIA) imparts offspring with anxiety- and depression-like behavior. By integrating bulk and single-nucleus RNA sequencing (snRNA-seq) with genome-wide 5hmC (5-hydroxymethylcytosine) profiling and 5mC (5-methylcytosine) profiling in prefrontal cortex (PFC) of ZIKV-affected male offspring mice, we revealed an overall loss of 5hmC and an increase of 5mC levels in intragenic regions, associated with transcriptional changes in neuropsychiatric disorder-related genes. In contrast to their rapid initiation and inactivation in normal conditions, immediate-early genes (IEGs) remain a sustained upregulation with enriched expression in excitatory neurons, which is coupled with increased 5hmC and decreased 5mC levels of IEGs in ZIKV-affected male offspring. Thus, MIA induces maladaptive methylome remodeling in brain and selectively regulates neuronal activity gene methylation linking to emotional behavioral abnormalities in offspring.

| S-EPMC10687003 | biostudies-literature

Haploinsufficiency, but not defective paternal 5mC oxidation, accounts for the developmental defects of maternal Tet3 knockouts

Project description:DNA demethylation of paternal genome in zygotes takes place in various mammals including mice and human. Recent studies have revealed that this is achieved through Tet3-mediated iterative oxidation of 5-methylcytosine (5mC) coupled with replication-dependent dilution. Tet3-mediated paternal DNA demethylation is believed to be required for mouse development given that Tet3 heterozygous embryos, derived by fertilizing Tet3 knockout (KO) oocytes with wild-type (WT) sperms, exhibit 5mC oxidation defects and embryonic sublethality, Here we demonstrate that the sublethality phenotype of the maternal KO mice is caused by haploinsufficiency of Tet3, but not by defective paternal 5mC oxidation. We found that Tet3 heterozygous mice derived from crosses of heterozygous father or mother with WT mice also exhibit sublethality phenotype similarly to Tet3 maternal KO mice. Importantly, embryos reconstituted with WT paternal nuclei that bypassed 5mC oxidation develop to term and grow to adulthood normally. Genome-scale DNA methylation analysis of the maternal KO zygotes and blastocysts demonstrated that hypermethylation caused by the depletion of maternal Tet3 is largely diminished by the blastocyst stage. Our study thus not only demonstrates that Tet3-mediated paternal 5mC oxidation is dispensable for mouse development but also suggests the existence of a compensation mechanism in preimplantation embryos that can compensate for the defective 5mC oxidation in zygotes. This data set includes RRBS data of wild-type and maternal Tet3 KO zygotes and blastocysts (C57BL/6J x CAST/EiJ)

2015-02-28 | E-GEOD-62719 | biostudies-arrayexpress

Neuronal Methylome in Multiple Sclerosis

Project description:Neuronal Methylome in Multiple Sclerosis

| PRJNA489474 | ENA