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Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE148120 | GEO | 2020/10/26

REPOSITORIES: GEO

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Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells [RNA-seq]

Project description:Using bisulfite padlock probes, mRNA sequencing, and hydroxymethylcytosine pull-down sequencing, we show that TET2 loss particularly influences DNA methylation (5mC) and hydroxymethylation (5hmC) patterns at erythroid gene enhancers and is associated with down-regulation of erythroid gene expression in the human erythroleukemia cell line TF-1. We show that 5-Aza disproportionately induces expression of these down regulated genes in TET2KO cells and that this effect may be related to 5mC changes at erythroid gene enhancers after 5-Aza exposure. This work highlights the role of 5mC and 5hmC changes at distal regulatory elements in regulating the expression of differentiation-associated gene signatures, and sheds light on how 5-Aza may be more effective in patients harboring TET2 mutations.

2020-10-26 | GSE148010 | GEO

Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells [HMCP-Seq]

2020-10-26 | GSE148119 | GEO

Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells [Bisulfite-seq]

2020-10-26 | GSE148012 | GEO

Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells

Project description:Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells

| PRJNA623289 | ENA

5-Azacytidine Transiently Restores Dysregulated Erythroid Differentiation Gene Expression in TET2-Deficient Erythroleukemia Cells.

Project description:DNA methyltransferase inhibitors (DNMTI) like 5-Azacytidine (5-Aza) are the only disease-modifying drugs approved for the treatment of higher-risk myelodysplastic syndromes (MDS), however less than 50% of patients respond, and there are no predictors of response with clinical utility. Somatic mutations in the DNA methylation regulating gene tet-methylcytosine dioxygenase 2 (TET2) are associated with response to DNMTIs, however the mechanisms responsible for this association remain unknown. Using bisulfite padlock probes, mRNA sequencing, and hydroxymethylcytosine pull-down sequencing at several time points throughout 5-Aza treatment, we show that TET2 loss particularly influences DNA methylation (5mC) and hydroxymethylation (5hmC) patterns at erythroid gene enhancers and is associated with downregulation of erythroid gene expression in the human erythroleukemia cell line TF-1. 5-Aza disproportionately induces expression of these down-regulated genes in TET2KO cells and this effect is related to dynamic 5mC changes at erythroid gene enhancers after 5-Aza exposure. We identified differences in remethylation kinetics after 5-Aza exposure for several types of genomic regulatory elements, with distal enhancers exhibiting longer-lasting 5mC changes than other regions. This work highlights the role of 5mC and 5hmC dynamics at distal enhancers in regulating the expression of differentiation-associated gene signatures, and sheds light on how 5-Aza may be more effective in patients harboring TET2 mutations. IMPLICATIONS: TET2 loss in erythroleukemia cells induces hypermethylation and impaired expression of erythroid differentiation genes which can be specifically counteracted by 5-Azacytidine, providing a potential mechanism for the increased efficacy of 5-Aza in TET2-mutant patients with MDS. VISUAL OVERVIEW: http://mcr.aacrjournals.org/content/molcanres/19/3/451/F1.large.jpg.

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Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells [RNA-seq]

Project description:Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells [RNA-seq]

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Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells [HMCP-Seq]

Project description:Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells [HMCP-Seq]

| PRJNA623294 | ENA

Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells [Bisulfite-seq]

Project description:Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells [Bisulfite-seq]

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The dysregulated <i>Pink1<sup>-</sup> Drosophila</i> mitochondrial proteome is partially corrected with exercise.

Project description:One of the genes which has been linked to the onset of juvenile/early onset Parkinson's disease (PD) is PINK1. There is evidence that supports the therapeutic potential of exercise in the alleviation of PD symptoms. It is possible that exercise may enhance synaptic plasticity, protect against neuro-inflammation and modulate L-Dopa regulated signalling pathways. We explored the effects of exercise on Pink1 deficient Drosophila melanogaster which undergo neurodegeneration and muscle degeneration. We used a 'power-tower' type exercise platform to deliver exercise activity to Pink1- and age matched wild-type Drosophila. Mitochondrial proteomic profiles responding to exercise were obtained. Of the 516 proteins identified, 105 proteins had different levels between Pink1- and wild-type non-exercised Drosophila. Gene ontology enrichment analysis and STRING network analysis highlighted proteins and pathways with altered expression within the mitochondrial proteome. Comparison of the Pink1- exercised proteome to wild-type proteomes showed that exercising the Pink1- Drosophila caused their proteomic profile to return towards wild-type levels.

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TET2 loss-of-function mutations associate with a DNA hypermethylation signature in diffuse large B-cell lymphoma

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-10-10 | E-GEOD-37365 | biostudies-arrayexpress