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MYCN directly regulates TET1 expression to control 5-hmC distribution and enhance neuroblastoma cell migration in hypoxia [hMe-SEAL]

ABSTRACT: MYCN directly regulates TET1 expression to control 5-hmC distribution and enhance neuroblastoma cell migration in hypoxia [hMe-SEAL]

PROVIDER: PRJNA704701 | ENA |

REPOSITORIES: ENA

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Role of Tet1 and Tet3 genes and Chromatin Remodeling in Cerebellar Circuit Formation [hMe-Seal]

Project description:Although mechanisms underlying early steps in cerebellar development are known, evidence is lacking on genetic and epigenetic changes during the establishment of the synaptic circuitry. Using metagene analysis, we report pivotal changes in multiple reactomes of epigenetic pathway genes in cerebellar granule cells (GCs) during circuit formation. During this stage, Tet genes are up-regulated and vitamin C activation of Tet enzymes increases the levels of 5-hydroxymethylcytosine (5hmC) at exon start sites of up-regulated genes, notably axon guidance genes and ion channel genes. Knockdown of Tet1 and Tet3 by RNA interference in ex vivo cerebellar slice cultures inhibits dendritic arborization of developing GCs, a critical step in circuit formation. These findings demonstrate a role for Tet genes and chromatin remodeling genes in the formation of cerebellar circuitry. 5hmC-enriched genomic DNA fragments were purified with a selective labeling strategy known as hMe-Seal and carried out DNA deep sequencing using Illumina HiSeq 2500.

2015-10-31 | E-GEOD-74401 | biostudies-arrayexpress

MYCN directly regulates TET1 expression to control 5-hmC distribution and enhance neuroblastoma cell migration in hypoxia [hMe-SEAL]

Project description:We characterized genome-wide 5-hydroxymerhylcytosine (5-hmC) distribution at 0,6,12,24, 48, 72 hours in hypoxia in SK-N-BE(2) neuroblastoma cell line.5-hmC increases over time in hypoxic but especially between 0 and 6 and 24 to 48 hours.

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

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Metabolic changes during human adipocyte differentiation promote stable DNA hydroxymethylation and binding of acetylated NEIL1 to adipogenic enhancers [hMe-Seal]

Project description:In the present study, we applied two whole-genome sequencing techniques (WGBS/oxBS and hMe-Seal) to detect 5hmC (and 5mC) changes during the differentiation of the human SGBS preadipocyte cell line to mature adipocytes. As technical and biological validation we performed BS and oxBS followed by 450k array analysis. RNA-seq data was performed in parallel to study transcriptional changes associated with differential hydroxymethylation. In human white adipose tissue (WAT) hydroxymethylation (hME-Seal) was characterized in comparison with histone modifications and acNEIL1 binding (ACT-seq).

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MYCN directly regulates TET1 expression to control 5-hmC distribution and enhance neuroblastoma cell migration in hypoxia

Project description:MYCN directly regulates TET1 expression to control 5-hmC distribution and enhance neuroblastoma cell migration in hypoxia

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Project description:MYCN directly regulates TET1 expression to control 5-hmC distribution and enhance neuroblastoma cell migration in hypoxia [RNA-Seq]

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Combined loss of Tet1 and Tet2 promotes B-cell, but not myeloid malignancies in mice

Project description:TET1/2/3 are methylcytosine dioxygenases regulating cytosine hydroxymethylation in the genome. Tet1 and Tet2 are abundantly expressed in HSC/HPCs and implicated in the pathogenesis of hematological malignancies. Tet2-deletion in mice causes myeloid malignancies, while Tet1-null mice develop B-cell lymphoma after an extended period of latency. Interestingly, TET1 and TET2 were often concomitantly down-regulated in acute B-lymphocytic leukemia. Here, we investigated the overlapping and non-redundant functions of Tet1/Tet2 in HSC maintenance and development of hematological malignancies using Tet1/2 double knockout (DKO) mice. DKO and Tet2-/- HSC/HPCs had overlapping and unique 5hmC and 5mC profiles and behaved differently. DKO mice exhibited strikingly decreased incidence and delayed onset of myeloid malignancies compared to Tet2-/- mice and in contrast developed lethal B-cell malignancies. Transcriptome analysis of DKO tumors revealed expression changes in many genes dysregulated in human B-cell malignancies, such as LMO2, BCL6 and MYC. These results highlight the critical roles of TET1 or TET2 individually and their cross-talks in the pathogenesis of hematological malignancies. Given the role of Tet proteins in 5mC oxidation, we employed a previously established chemical labeling and affinity purification method coupled with high-throughput sequencing (hMe-Seal) to profile the genome-wide distribution of 5hmC, as well as methylated DNA immunoprecipitation (MeDIP) coupled with high-throughput sequencing (MeDIP-seq) to profile 5mC using BM LK cells purified from young WT, Tet2-/- and DKO mice (6-10 wks old).

2015-11-12 | E-GEOD-73611 | biostudies-arrayexpress

Tet1 and hydroxymethylcytosine in transcription and DNA methylation fidelity (ChIP/DIP-Seq data)

Project description:We analyzed the genome-wide binding of Tet1 in control (shScr) and Tet1 knockdown (shTet1) mouse ES cells using two different Tet1 antibodies (Tet1-C and Tet1-N). Furthermore, we generated genome-wide mapping of hydroxymethyl cytosine (hmC) and methyl cytosine (mC). We find that hmC, in contrast to mC, is also found at transcription start sites (TSSs), and that there is a significant overlap between Tet1 binding and hmC positive regions. Surprisingly, our results also suggest, that Tet1 has a role in transcriptional repression. We showed that Tet1 associates with Sin3A co-repressor complex, and by performing ChIP-sequencing of Sin3A, we find co-localisation of Tet1 and Sin3a throughout the genome Examination of Tet1 and Sin3A binding as well as hmC and mC localization in mouse ES cells

2011-04-13 | E-GEOD-24841 | biostudies-arrayexpress

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