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Novel Isoforms of the Epigenetic Regulator TET1 Differentially Control CNS Synaptic Function, Plasticity, and Cognition

ABSTRACT: Novel Isoforms of the Epigenetic Regulator TET1 Differentially Control CNS Synaptic Function, Plasticity, and Cognition

PROVIDER: PRJNA588473 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10423700_1.fastq.gz	Fastqsanger.gz
	SRR10423700_2.fastq.gz	Fastqsanger.gz
	SRR10423701_1.fastq.gz	Fastqsanger.gz
	SRR10423701_2.fastq.gz	Fastqsanger.gz
	SRR10423702_1.fastq.gz	Fastqsanger.gz

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Novel Isoforms of the Epigenetic Regulator TET1 Differentially Control CNS Synaptic Function, Plasticity, and Cognition

Project description:Two distinct Tet1 isoforms are expressed, one encoding full-length TET1 (Tet1L) and the other a truncated transcript (Tet1S), lacking a large portion of the N-terminus. Each isoform displays unique transcriptional regulation, subcellular protein localization and enzymatic activity. In neurons, Tet1L and Tet1S govern the expression and methylation levels of distinct gene ensembles that when disrupted.

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Project description:Synapse formation is a dynamic process essential for neuronal circuit development and maturation. At the synaptic cleft, trans-synaptic protein-protein interactions constitute major biological determinants of proper synapse efficacy. The balance of excitatory and inhibitory synaptic transmission (E-I balance) stabilizes synaptic activity and its dysregulation has been implicated in neurodevelopmental disorders including autism spectrum disorders. However, the molecular mechanisms underlying E-I balance remains to be elucidated. Here, we investigate Neuroligin (Nlgn) genes which encode a family of postsynaptic adhesion molecules that shape excitatory and inhibitory synaptic function. We identified that NLGN3 protein differentially regulates inhibitory synaptic transmission in a splice isoform-dependent manner in hippocampal CA1 synapses. Distinct subcellular localization patterns of NLGN3 isoforms contribute to the functional differences observed among splice variants. Finally, our single-cell sequencing analysis reveals that Nlgn1 and Nlgn3 are the major Nlgn genes and that Nlgn splice isoforms are highly diverse in CA1 pyramidal neurons.

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Project description:DNA hydroxymethylation by epigenetic modifiers TET dioxygenases is critical for gene transcription in various biological processes, however, its role in oligodendrocyte maturation and functions remain elusive. Here, we found that mice lacking Tet1 in the oligodendrocyte lineage exhibited hypomyelination in the CNS in the juvenile stage, leading to defects in action potential propagation, motor coordination, anxiety-like behavior and spatial memory capacities. Although the myelin deficiency recovered in adulthood, remyelination after cuprizone-induced demyelination was compromised in Tet1cKO mice. By integrating transcriptome and DNA methylation profiles, we identified a cohort of genes that were differentially regulated by Tet1 and hyperhydroxymethylation, including the genes associated with Ca2+ transportation. Tet1-deficient OPCs exhibited a reduction in [Ca2+] oscillations, while the agonists of calcium internal stores rescued the differentiation defect of Tet1-deficient OPCs. Thus, our results suggest that stage-specific Tet1-mediated epigenetic programming in oligodendrocytes maintain Ca2+ homeostasis for differentiation and regulate neuronal activities and myelin repair.

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Project description:Using RNA sequencing, we found that Tet1 alters gene expression. Mechanistically, we found that Tet1 deficiency leads to the abnormal Ca2+ signaling by regulating the expression of GluA1, which can be rescued by ectectopic expression of GluA1. Collectively, our findings suggest that Tet1 plays important functions by regulating astrocytes Ca2+ signaling.

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Project description:Tet (Ten eleven translocation) mediated 5-hydroxymethylcytosine (5hmC) is highly enriched in the neuronal system and is involved in diverse biological processes and diseases. However, the function of 5hmC in astrocytes remains completely unknown. In the present study, we show that Tet1 deficiency alters astrocytes morphology and impairs neuronal function. Specific deletion of Tet1 in astrocytes impairs learning and memory ability of mice. Using 5hmC high-throughput DNA sequencing and RNA sequencing, we found the distribution feature of 5hmC in astrocytes and that Tet1 deficiency induces DNA hydroxymethylation regions (DhMRs) and alters gene expression. Mechanistically, we found that Tet1 deficiency leads to the abnormal Ca2+ signaling by regulating the expression of GluA1, which can be rescued by ectectopic expression of GluA1. Collectively, our findings suggest that Tet1 plays important functions by regulating astrocytes Ca2+ signaling.

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2020-11-03 | MTBLS1952 | MetaboLights

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