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Astrocytes Tet1 regulates neuronal development and cognition through modulating GluA1

ABSTRACT: Astrocytes Tet1 regulates neuronal development and cognition through modulating GluA1

PROVIDER: PRJNA688636 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13327759_1.fastq.gz	Fastqsanger.gz
	SRR13327759_2.fastq.gz	Fastqsanger.gz
	SRR13327760_1.fastq.gz	Fastqsanger.gz
	SRR13327760_2.fastq.gz	Fastqsanger.gz
	SRR13327761_1.fastq.gz	Fastqsanger.gz

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Astrocytes Tet1 regulates neuronal development and cognition through modulating GluA1 in mice

Project description:Astrocytes Tet1 regulates neuronal development and cognition through modulating GluA1 in mice

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Astrocytes Tet1 regulates neuronal development and cognition through modulating GluA1 in mice

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.

2021-11-17 | GSE165370 | GEO

Astrocytes Tet1 regulates neuronal development and cognition through modulating GluA1

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.

2021-11-17 | GSE164025 | GEO

Direct Generation of Human Neuronal Cells from Adult Astrocytes by Small Molecules

Project description:Astrocytes, due to the proximity to neuronal lineage and capability to proliferate, are ideal starting cells to regenerate neurons. Human fetal astrocytes have been successfully converted into neuronal cells by small molecules, which offer a broader range of further applications than transcription factor-mediated neuronal reprogramming. Here we report human adult astrocytes could also be converted into neuronal cells by a different set with fewer small molecules. These induced neuronal cells exhibited typical neuronal morphologies, expressed neuronal markers, and displayed neuronal electrophysiological properties. Genome-wide RNA-sequencing analysis showed the gene expression profile of induced neuronal cells resembled that of human embryonic stem cell-differentiated neurons. When transplanted into postnatal mouse brains, these induced neuronal cells could survive in vivo. Altogether, our study provides a new strategy to directly generate transgene-free neurons from human adult astrocytes by small molecules.

2017-06-12 | GSE84826 | GEO

Fetal Growth Restriction Impairs Hippocampal Neurogenesis and Cognition via Tet1 in Offspring

Project description:Fetal Growth Restriction Impairs Hippocampal Neurogenesis and Cognition via Tet1 in Offspring

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Disease-relevant upregulation of P2Y1 receptor in astrocytes enhances neuronal excitability via IGFBP2

Project description:Reactive astrocytes play a pivotal role in the pathogenesis of neurological diseases; however, their functional phenotype and the downstream molecules by which they modify disease pathogenesis remain unclear. Here, we genetically increase P2Y1 receptor (P2Y1R) expression, which is upregulated in reactive astrocytes in several neurological diseases, in astrocytes of male mice to explore its function and the downstream molecule. This astrocyte-specific P2Y1R overexpression causes neuronal hyperexcitability by increasing both astrocytic and neuronal Ca2+ signals. We identify insulin-like growth factor-binding protein 2 (IGFBP2) as a downstream molecule of P2Y1R in astrocytes; IGFBP2 acts as an excitatory signal to cause neuronal excitation. In neurological disease models of epilepsy and stroke, reactive astrocytes upregulate P2Y1R and increase IGFBP2. The present findings identify a mechanism underlying astrocyte-driven neuronal hyperexcitability, which is likely to be shared by several neurological disorders, providing insights that might be relevant for intervention in diverse neurological disorders.

2024-05-17 | GSE242450 | GEO

MBD1 activates neuronal developmental genes through modulating chromatin structure during neuronal maturation

Project description:MBD1 activates neuronal developmental genes through modulating chromatin structure during neuronal maturation

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FOXA1 potentiates lineage-specific enhancer activation through modulating TET1 expression and function

Project description:FOXA1 is a FKHD family protein that translates epigenetic signatures at target enhancers to lineage-specific transcription and differentiation. Through genome-wide location analyses, here we show that FOXA1 expression and occupancy are, in turn, required for the maintenance of this epigenetic signature, namely DNA hypomethylation and histone 3 lysine 4 methylation. Mechanistically, this involves TET1, a 5-methylcytosine dioxygenase. We found that FOXA1 induces TET1 expression via direct binding at its cis-regulatory elements. Further, FOXA1 physically interacts with the TET1 protein through its CXXC domain. TET1 thus co-occupies FOXA1-dependent enhancers and mediates local DNA demethylation and concomitant histone 3 lysine 4 methylation, further potentiating FOXA1 recruitment. FOXA1 binding events were markedly reduced following TET1 depletion. Together, our results support that FOXA1 is not only a reader, but also a writer, of the epigenetic signatures at lineage-specific enhancers and that TET1 and FOXA1 form a feed-forward regulatory loop for enhancer activation. ChIP-Seq examination of FOXA1 binding sites in LNCaP cell, and epigenetic markers (5mC, 5hmC, H3K4me2) profiling upon TET1 depletion

2016-07-22 | E-GEOD-73363 | biostudies-arrayexpress

A Novel TET1 Based Complex Controls DNA Repair Genes by Modulating H4K16 Acetylation In response to oxidative damage [RRBS]

Project description:TET1, in addition its function as a DNA demethylase, plays important roles in both transcriptional repression and activation. However, the underlying mechanism how TET1 functions in transcriptional regulation remains elusive. Here, by integrative genomic and biochemical studies, we demonstrate that TET1 forms a novel chromatin modifying complex with hMOF, SIRT1, and the scaffold protein SIN3A to specifically regulate DNA repair genes by modulating H4K16 acetylation. Dynamic recomposition of this complex induced by oxidative damage, characterized as dissociation of TET1 and hMOF or increased binding of SIRT1, leads to hypoacetylation of H4K16 to repress the expression of DNA repair genes. Importantly, similar recomposition of this complex was validated in an oncogenic transformation cell line, which further endorsed that the role of this complex was involved in tumorigenesis. Our findings reveal a novel mechanism for TET1 to modulate H4K16ac by chromatin recomposition, with which TET1 regulates the expression of DNA repair genes instead of its well-known role in DNA demethylation.

2017-03-01 | GSE66395 | GEO

TET1 interactome in mESCs (via ChIP-MS)

Project description:Precise regulation of DNA methylation in mammals is critical for genome stability and epigenetic regulation. The discovery of the ten-eleven translocation (TET) proteins catalyzing the oxidation from 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC), and 5-carboxylcytosine (5caC) revolutionized the perspective on the complexity and regulation of DNA modifications. Despite accumulating knowledge about the role of TET1, it remains unclear to what extent these can be attributed to its catalytic activity. Here, we use genome engineering and quantitative multi-omics approaches to dissect the role and mechanism of TET1 in mESCs. Our study identifies TET1 as an essential interaction hub for multiple chromatin modifying complexes and as a global regulator of histone modifications. Strikingly, we find that the majority of transcriptional regulation depends on non-catalytic functions of TET1. Moreover, we show that the establishment of H3K9me3 and H4K20me3 at ERV1, ERVK, and ERVL is mediated by TET1 independent of DNA demethylation. We provide evidence that repression of endogenous retroviruses depends on the interaction between TET1 and SIN3A. In summary, we demonstrate that the non-catalytic functions of TET1 are critical for regulation of gene expression and the silencing of endogenous retroviruses in mESCs.

2022-08-31 | PXD028850 | Pride

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