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Epigenomic analysis of Parkinson's disease neurons identifies TET2 loss as neuroprotective

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

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE136010 | GEO | 2020/06/19

REPOSITORIES: GEO

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Epigenomic analysis of Parkinson's disease neurons identifies TET2 loss as neuroprotective

Project description:Epigenomic analysis of Parkinson's disease neurons identifies TET2 loss as neuroprotective

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Epigenomic analysis of Parkinson’s disease neurons identifies TET2 loss as neuroprotective [PD_TET2_Bisulfite_Padlock_Seq]

Project description:Epigenetic control of enhancers is centrally involved in modifying neuronal functions and may contribute to Parkinson's disease (PD) pathogenesis. Here, we comprehensively profile DNA methylation at enhancers genome-wide in neurons of 57 PD patients and 48 healthy individuals. There is a widespread increase in cytosine modifications at enhancers in PD neurons, which is partly due to elevated hydroxymethylation levels. Epigenetic dysregulation of enhancers in PD converge on transcriptional abnormalities affecting neuronal signaling and immune activation pathways. In particular, PD patients exhibit an epigenetic and transcriptional upregulation of TET2, a master-regulator of cytosine modification status. TET2 inactivation in a neuronal cell line enriches for cytosine modification changes that are reciprocal to those observed in PD neurons. Furthermore, Tet2 inactivation in mice fully prevents dopaminergic neuronal loss in the substantia nigra induced by prior inflammation. Tet2 loss in mice also attenuates transcriptional immune responses to an inflammatory trigger. Thus, widespread epigenetic dysregulation of enhancers in PD neurons may, in part, be mediated by increased TET2 expression. Decreased Tet2 activity is neuroprotective, in vivo, and may be a novel therapeutic target for PD.

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Epigenomic analysis of Parkinson’s disease neurons identifies TET2 loss as neuroprotective [PD_hMeDIP_Seq]

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Epigenomic analysis of Parkinson’s disease neurons identifies TET2 loss as neuroprotective [TET2_LPS_RNA_Seq]

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Epigenomic analysis of Parkinson’s disease neurons identifies TET2 loss as neuroprotective [TET2i_Bisulfite_Padlock_seq]

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Epigenomic analysis of Parkinson’s disease neurons identifies TET2 loss as neuroprotective [TET2i_Bisulfite_Padlock_seq]

Project description:Epigenomic analysis of Parkinson’s disease neurons identifies TET2 loss as neuroprotective [TET2i_Bisulfite_Padlock_seq]

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Epigenomic analysis of Parkinson’s disease neurons identifies TET2 loss as neuroprotective [PD_hMeDIP_Seq]

Project description:Epigenomic analysis of Parkinson’s disease neurons identifies TET2 loss as neuroprotective [PD_hMeDIP_Seq]

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Epigenomic analysis of Parkinson’s disease neurons identifies TET2 loss as neuroprotective [PD_TET2_Bisulfite_Padlock_Seq]

Project description:Epigenomic analysis of Parkinson’s disease neurons identifies TET2 loss as neuroprotective [PD_TET2_Bisulfite_Padlock_Seq]

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Epigenomic analysis of Parkinson’s disease neurons identifies TET2 loss as neuroprotective [TET2_LPS_RNA_Seq]

Project description:Epigenomic analysis of Parkinson’s disease neurons identifies TET2 loss as neuroprotective [TET2_LPS_RNA_Seq]

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Hypothesis-based RNAi screening identifies neuroprotective genes in a Parkinson's disease model.

Project description:Genomic multiplication of the locus-encoding human alpha-synuclein (alpha-syn), a polypeptide with a propensity toward intracellular misfolding, results in Parkinson's disease (PD). Here we report the results from systematic screening of nearly 900 candidate genetic targets, prioritized by bioinformatic associations to existing PD genes and pathways, via RNAi knockdown. Depletion of 20 gene products reproducibly enhanced misfolding of alpha-syn over the course of aging in the nematode Caenorhabditis elegans. Subsequent functional analysis of seven positive targets revealed five previously unreported gene products that significantly protect against age- and dose-dependent alpha-syn-induced degeneration in the dopamine neurons of transgenic worms. These include two trafficking proteins, a conserved cellular scaffold-type protein that modulates G protein signaling, a protein of unknown function, and one gene reported to cause neurodegeneration in knockout mice. These data represent putative genetic susceptibility loci and potential therapeutic targets for PD, a movement disorder affecting approximately 2% of the population over 65 years of age.

| S-EPMC2206604 | biostudies-literature

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