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Stress modulates Ahi1-dependent nuclear localization of Ten-Eleven Translocation Protein 2

ABSTRACT: Stress modulates Ahi1-dependent nuclear localization of Ten-Eleven Translocation Protein 2

PROVIDER: PRJNA704360 | ENA |

REPOSITORIES: ENA

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Stress modulates Ahi1-dependent nuclear localization of Ten-Eleven Translocation Protein 2

Project description:Three Ten-Eleven Translocation (Tet) enzymes are epigenetic regulators of gene expression that promote 5-hydroxymethylcytosine (5hmC) modification of genes. Here, we show that the loss of Tet2 can induce depression-like phenotypes in mice. Paradoxically, using the paradigms of chronic stress, such as chronic mild stress (CMS) and chronic social defeat stress (CSDS), we found that depressive behaviors were associated with increased Tet2 expression but decreased global 5hmC level in hippocampus. We examined the genome-wide 5hmC profile in the hippocampus of Tet2 knockout mice and identified 651 dynamically hydroxymethylated regions, 31 of which overlapped with known depression-associated loci. We further showed that chronic stress could induce the abnormal nuclear translocation of Tet2 protein from cytosol. Through Tet2 immunoprecipitation and mass spectrum analyses, we identified a cellular trafficking protein, Abelson helper integration site-1 (Ahi1), which could interact with Tet2 protein. Ahi1 knockout or knockdown caused the accumulation of Tet2 in cytosol. The reduction of Ahi1 protein under chronic stress explained the abnormal Ahi1-dependent nuclear translocation of Tet2. These findings together provide the evidence for a critical role of modulating Tet2 nuclear translocation in regulating stress response.

2021-11-22 | GSE167344 | GEO

Stress modulates Ahi1-dependent nuclear localization of ten-eleven translocation protein 2.

Project description: Not available

| S-EPMC8837822 | biostudies-literature

Ten-eleven translocation proteins modulate the response to environmental stress in mice

Project description:Ten-eleven translocation proteins modulate the response to environmental stress in mice

| PRJNA415948 | ENA

Loss of Ten-Eleven Translocation 2 Exacerbates allergic inflammation by 5-Hydroxymethylcytosine Remodeling in Immunologic Pathways

Project description:Here we show that loss of ten-eleven translocation protein (Tet2) could impact the severity of allergic rhinitis (AR) in ovalbumin-induced mouse model. Genome-wide 5hmC profiling of wildtype, Tet2+/- and Tet2-/- mice in response to AR revealed that the loss of Tet2 could lead to the 5hmC alteration at specific immune response genes on RNA-seq.

2021-03-29 | GSE171005 | GEO

Ten-eleven translocation proteins modulate the response to environmental stress in mice

Project description:5-hydroxymethylcytosine (5hmC) is enriched in brain and has been recognized as an important DNA modification. However, the roles of 5hmC and its “writers”, Ten-eleven translocation (Tet) proteins, in stress-induced response have yet to be elucidated. Here, we show that chronic restraint stress (CRS) induced the depression-like behavior in mice and resulted in a 5hmC reduction in prefrontal cortex (PFC). Interestingly, we found that the loss of Tet1 (Tet1 KO) led to the resistance to CRS while the loss of Tet2 (Tet2 KO) increased the susceptibility of mice to CRS. Genome-wide 5hmC profiling identified the phenotype associated stress-induced dynamically hydroxymethylated loci (PA-SI-DhML), which are strongly enriched with hypoxia-induced factor (HIF) binding motifs. We demonstrated the physical interaction between TET1 and HIF1α induced by CRS, and revealed that the increased HIF1α binding under CRS is associated with SI-DhML. These results together suggest that TET1 could regulate stress-induced response by interacting with HIF1α.

2018-11-21 | GSE106220 | GEO

Loss of Ten-Eleven Translocation 2 Exacerbates allergic inflammation by 5-Hydroxymethylcytosine Remodeling in Immunologic Pathways

Project description:Loss of Ten-Eleven Translocation 2 Exacerbates allergic inflammation by 5-Hydroxymethylcytosine Remodeling in Immunologic Pathways

| PRJNA718078 | ENA

Ten-eleven translocation protein 1 modulates medulloblastoma progression.

Project description: Not available

| S-EPMC8082834 | biostudies-literature

Genes regulated by both of Ten-Eleven translocation 3 and Tumor necrosis factor α in Rheumatoid arthritis fibroblast-like synoviocytes

Project description:As DNA demethylation is a dynamic epigenetic regulation in pattern formation of DNA methylation, we reasoned that DNA demethylation facilitates Rheumatoid arthritis (RA) progression. To address this point, we picked up the DNA dioxygenase family members (Ten-Eleven translocation: TET1/2/3) as these enzymes conduct the prime process of DNA demethylaion. Tumor necrosis factor α (TNFα) , one of the pro-inflammatory cytokines, was found effective in up-regulation in TET3 level in the cultured fibroblast-like synoviocytes (FLS), and the stimulated FLS cells exhibited high cell mobility with gene induction of cell-migration related factors in a TET3-dependent manner. From our findings, we presume that DNA demethylation mediated TET3 facilitates RA progression and chronicity as an epigenetic regulation.

2021-02-09 | GSE166389 | GEO

Ten-Eleven Translocation 2 regulates adult neurogenesis through modulating 5mC oxidation dynamics at distinct regulatory elements

Project description:Emerging evidence suggests that various epigenetic mechanisms play important roles in regulating adult neurogenesis. Ten-Eleven Translocation (Tet) proteins, the 5mC dioxygenases, could convert 5mC stepwise to 5-hydroxymethylcytosine (5hmC) and its further oxidation products, which constitute active DNA demethylation pathway. Here we show that unlike embryonic stem cells, 5hmC is acquired upon differentiation of adult neural stem cells (NSCs). The loss of Tet2 in proliferating NSCs significantly decreases their 5hmC abundance and partially blocks the acquisition of 5hmC upon differentiation, leading to the increased proliferation and reduced differentiation both in vitro and in vivo. This impaired neurogenesis process results in a defect of learning and memory as well as depressive behavior in Tet2-/- animals. Biochemical and epigenomic analyses reveal that transcription factor Forkhead box O3 (Foxo3a) physically interacts with Tet2 and orchestrates with various forms cytosine modifications to regulate different cohorts of gene expression through distinct mechanisms. These data together establish a novel and fundamental role of Tet2 in neurogenesis by coordinating with Foxo3a to epigenetically regulate the expression of key genes involved in neurogenesis.

2017-07-03 | GSE65994 | GEO

Ten-eleven translocation (Tet) methylcytosine dioxygenases dependent viral DNA demethylation mediates in vivo hepatitis B virus (HBV) biosynthesis

Project description:Liver-specific ten-eleven translocation methylcytosine dioxygenases 2 and 3 (Tet2 plus Tet3)-deficient hepatitis B virus (HBV) transgenic mice fail to support viral biosynthesis. The levels of viral transcription and replication intermediates are dramatically reduced. Hepatitis B core antigen (HBcAg) is only observed in a very limited number of pericentral hepatocytes in a pattern that is similar to glutamate-ammonia ligase (Glul), a -catenin target gene. HBV transcript abundance in Tet-deficient mice resembles that observed in wild-type neonatal mice. Furthermore, the RNA levels of several -catenin target genes including Glul, Lhpp, Notun, Oat, Slc1a2 and Tbx3, in Tet-deficient mice was also similar to that observed in wild-type neonatal mice. As HBV transcription is regulated by -catenin, these finding support the suggestion that neonatal Tet-deficiency might limit -catenin target gene expression, limiting viral biosynthesis. Additionally, HBV transgene DNA displays increased 5-methylcytosine (5mC) frequency at CpG sequences consistent with neonatal Tet-deficiency being responsible for decreased developmental viral DNA demethylation mediated by 5mC oxidation to 5-hydroxymethylcytosine (5hmC), a process that might be responsible for the reduction in cellular -catenin target gene expression and viral transcription and replication.

2023-11-29 | GSE242448 | GEO

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