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HIF-1 directly induces TET3 expression to redistribute 5-hydroxymethylcytosine and induce erythroid gene expression in hypoxia

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE142870 | GEO | 2020/02/01

REPOSITORIES: GEO

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HIF-1 directly induces TET3 expression to redistribute 5-hydroxymethylcytosine and induce erythroid gene expression in hypoxia [5-hmC]

Project description:We characterized genome-wide 5-hydroxymerhylcytosine (5-hmC) distribution of CD34+ cells undergoing erythroid differentiation in normoxia vs. hypoxia by chemically labeling 5-hmC followed by pull-down and sequencing (hMe-SEAL). We found that hypoxia increases both the number and the prominance of 5-hmC peaks at each time point, especially at day 7 and 10.

2020-02-01 | GSE142869 | GEO

HIF-1 directly induces TET3 expression to redistribute 5-hydroxymethylcytosine and induce erythroid gene expression in hypoxia [RNA-seq]

Project description:We performed RNA-sequencing on erythropoietic cells cultured in normoxia or hypoxia at days 3,7, and 10. We found numerous expression changes induced by hypoxia, including the canonical hypoxia targets as well as a number of genes encoding genes involved in epigenetic processes.

2020-02-01 | GSE142867 | GEO

HIF-1 directly induces TET3 expression to redistribute 5-hydroxymethylcytosine and induce erythroid gene expression in hypoxia [ChIP-seq]

Project description:We performed HIF-1alpha ChIP-seq in K562 cells cultured in normoxia vs. hypoxia for 3 days. We identified two new HIF binding sites in TET3 intron 2 that control TET3 expression in hypoxia

2020-02-01 | GSE142865 | GEO

HIF-1 directly induces TET3 expression to enhance 5-hmC density and induce erythroid gene expression in hypoxia.

Project description:In mammalian cells, cytosines found within cytosine guanine dinucleotides can be methylated to 5-methylcytosine (5-mC) by DNA methyltransferases and further oxidized by the Ten-eleven translocation dioxygenase (TET) enzymes to 5-hydroxymethylcytosine (5-hmC). We have previously shown that hematopoietic stem and progenitor cells (HSPCs) with TET2 mutations have aberrant 5-hmC distribution and less erythroid differentiation potential. However, these experiments were performed under standard tissue culture conditions with 21% oxygen (O2), whereas HSPCs in human bone marrow reside in ∼1% O2. Therefore, to model human erythropoiesis more accurately, we compared 5-hmC distribution and gene expression in hypoxic vs normoxic conditions. Despite TET enzymes having limited O2 as a substrate in hypoxia, 5-hmC peaks were more numerous and pronounced than in normoxia. Among the TET genes, TET3 was upregulated specifically in hypoxia. We identified 2 HIF-1 binding sites in TET3 by chromatin immunoprecipitation of HIF-1α followed by sequencing, and TET3 upregulation was abrogated with deletion of both sites, indicating that TET3 is a direct HIF-1 target. Finally, we showed that loss of one or both of these HIF-1 binding sites in K562 cells disrupted erythroid differentiation in hypoxia and lowered cell viability. This work provides a molecular link between O2 availability, epigenetic modification of chromatin, and erythroid differentiation.

| S-EPMC7362358 | biostudies-literature

HIF-1 directly induces TET3 expression to redistribute 5-hydroxymethylcytosine and induce erythroid gene expression in hypoxia

Project description:HIF-1 directly induces TET3 expression to redistribute 5-hydroxymethylcytosine and induce erythroid gene expression in hypoxia

| PRJNA598714 | ENA

HIF-1 directly induces TET3 expression to redistribute 5-hydroxymethylcytosine and induce erythroid gene expression in hypoxia [ChIP-seq]

Project description:HIF-1 directly induces TET3 expression to redistribute 5-hydroxymethylcytosine and induce erythroid gene expression in hypoxia [ChIP-seq]

| PRJNA598710 | ENA

HIF-1 directly induces TET3 expression to redistribute 5-hydroxymethylcytosine and induce erythroid gene expression in hypoxia [RNA-seq]

Project description:HIF-1 directly induces TET3 expression to redistribute 5-hydroxymethylcytosine and induce erythroid gene expression in hypoxia [RNA-seq]

| PRJNA598712 | ENA

HIF-1 directly induces TET3 expression to redistribute 5-hydroxymethylcytosine and induce erythroid gene expression in hypoxia [5-hmC]

Project description:HIF-1 directly induces TET3 expression to redistribute 5-hydroxymethylcytosine and induce erythroid gene expression in hypoxia [5-hmC]

| PRJNA598718 | ENA

Moderate hypoxia induces β-cell dysfunction with HIF-1-independent gene expression changes.

Project description:Pancreatic β-cell failure is central to the development and progression of type 2 diabetes. We recently demonstrated that β-cells become hypoxic under high glucose conditions due to increased oxygen consumption and that the pancreatic islets of diabetic mice but not those of control mice are moderately hypoxic. However, the impact of moderate hypoxia on β-cell number and function is unknown. In the present study, moderate hypoxia induced a hypoxic response in MIN6 cells, as evidenced by increased levels of HIF-1α protein and target genes. Under these conditions, a selective downregulation of Mafa, Pdx1, Slc2a2, Ndufa5, Kcnj11, Ins1, Wfs1, Foxa2, and Neurod1, which play important roles in β-cells, was also observed in both MIN6 cells and isolated pancreatic islets. Consistent with the altered expression of these genes, abnormal insulin secretion was detected in hypoxic MIN6 cells. Most of the hypoxia-induced gene downregulation in MIN6 cells was not affected by the suppression of HIF-1α, suggesting a HIF-1-independent mechanism. Moderate hypoxia also induced apoptosis in MIN6 cells. These results suggest that hypoxia is a novel stressor of β-cells and that hypoxic stress may play a role in the deterioration of β-cell function.

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Neocortical Tet3-mediated accumulation of 5-hydroxymethylcytosine promotes rapid behavioral adaptation.

Project description:5-hydroxymethylcytosine (5-hmC) is a novel DNA modification that is highly enriched in the adult brain and dynamically regulated by neural activity. 5-hmC accumulates across the lifespan; however, the functional relevance of this change in 5-hmC and whether it is necessary for behavioral adaptation have not been fully elucidated. Moreover, although the ten-eleven translocation (Tet) family of enzymes is known to be essential for converting methylated DNA to 5-hmC, the role of individual Tet proteins in the adult cortex remains unclear. Using 5-hmC capture together with high-throughput DNA sequencing on individual mice, we show that fear extinction, an important form of reversal learning, leads to a dramatic genome-wide redistribution of 5-hmC within the infralimbic prefrontal cortex. Moreover, extinction learning-induced Tet3-mediated accumulation of 5-hmC is associated with the establishment of epigenetic states that promote gene expression and rapid behavioral adaptation.

| S-EPMC4024925 | biostudies-literature

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