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MicroRNA-29 is an essential regulator of non-CG methylation during brain maturation

ABSTRACT: MicroRNA-29 is an essential regulator of non-CG methylation during brain maturation

PROVIDER: PRJNA662952 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10423400_1.fastq.gz	Fastqsanger.gz
	SRR10423400_2.fastq.gz	Fastqsanger.gz
	SRR10423401_1.fastq.gz	Fastqsanger.gz
	SRR10423401_2.fastq.gz	Fastqsanger.gz
	SRR10423402_1.fastq.gz	Fastqsanger.gz

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MicroRNA-29 is an essential regulator of non-CG methylation during brain maturation [Bisulfite-seq]

Project description:While embryonic brain development and neurodegeneration have been examined extensively, the events that govern postnatal brain maturation are less understood. During this period, widespread changes in synaptic connectivity are evident1,2 and, perturbations of synaptic development or maturation can have severe neurobehavioral consequences as seen in autism spectrum disorders (ASD), epilepsy and schizophrenia3-6. Recent studies have led to the unexpected discovery that marked increases in non-canonical (non-CG) DNA methylation occur during postnatal brain maturation7-14. This de novo CH methylation (where H= A, C, T), which occurs 1-4 weeks postnatally in mice and 1-15 years in humans7, is important for experience-dependent fine tuning of gene expression15 . The critical period of CH methylation appears to be mediated by Dnmt3a, the DNA methyltransferase that catalyzes CH methylation8,9. During brain maturation, Dnmt3a levels are elevated and then sharply decline7,16, and a strict control of CH methylation seems important as mutations or variants of Dnmt3a are associated with ASD, epilepsy and intellectual disability17-19. Here we identify the microRNA miR-29 as an essential regulator of Dnmt3a and CH methylation during brain maturation. Mice deficient in miR-29 or mice in which miR-29 can no longer target Dnmt3a exhibit enhanced levels of Dnmt3a, global CH hypermethylation, and repression of neuronal genes specifically associated with synaptic activity and neurotransmission. Importantly, these mice appear normal at birth, but subsequently exhibit severe neurological deficits including susceptibility to seizures and premature lethality. Together, these results identify an essential function of miR-29 in defining the critical period of DNA methylation during brain maturation, the absence of which results in neurobehavioral deficits.

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MicroRNA-29 is an essential regulator of non-CG methylation during brain maturation [RNA-seq]

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MicroRNA-29 is an essential regulator of non-CG methylation during brain maturation [RNA-seq]

Project description:MicroRNA-29 is an essential regulator of non-CG methylation during brain maturation [RNA-seq]

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MicroRNA-29 is an essential regulator of non-CG methylation during brain maturation [Bisulfite-seq]

Project description:MicroRNA-29 is an essential regulator of non-CG methylation during brain maturation [Bisulfite-seq]

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USP18 is an essential regulator of muscle cell differentiation and maturation

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MicroRNA-29 is an essential regulator of non-CG methylation during brain maturation

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

2021-02-14 | GSE157842 | GEO

MicroRNA-29 is an essential regulator of brain maturation through regulation of CH methylation.

Project description:Although embryonic brain development and neurodegeneration have received considerable attention, the events that govern postnatal brain maturation are less understood. Here, we identify the miR-29 family to be strikingly induced during the late stages of brain maturation. Brain maturation is associated with a transient, postnatal period of de novo non-CG (CH) DNA methylation mediated by DNMT3A. We examine whether an important function of miR-29 during brain maturation is to restrict the period of CH methylation via its targeting of Dnmt3a. Deletion of miR-29 in the brain, or knockin mutations preventing miR-29 to specifically target Dnmt3a, result in increased DNMT3A expression, higher CH methylation, and repression of genes associated with neuronal activity and neuropsychiatric disorders. These mouse models also develop neurological deficits and premature lethality. Our results identify an essential role for miR-29 in restricting CH methylation in the brain and illustrate the importance of CH methylation regulation for normal brain maturation.

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