Unknown,Transcriptomics,Genomics,Proteomics

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ChIP-Seq data from Nup133 ChIP performed on primary male and female mouse derived oligodendrocyte precursor cells

ABSTRACT: Nup133 is known to play a crucial role in neural cell differentiation. But its downstream targets and the exact mechanisms of its action are largely unknown. Hence, we performed targeted chromatin immunoprecipitation experiments followed by next generation sequencing to identify its genomic targets. Mouse OPCs that were isolated separately from male and female littermates were subjected to ChIP using anti-rabbit NUP133 Polyclonal antibody. The prepared ChIP output DNA from 4 individual bio-replicates, along with an input control for each sample was used to prepare Illumina TruSeq nano ChIP sequencing libraries. The Illumina NextSeq 500 platform and a high-output v2 1x75bp cycles kit were used to sequence the Illumina TruSeq ChIP libraries.

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Mus musculus

SUBMITTER: Matthias Heckmann

PROVIDER: E-MTAB-7332 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Nup133 and ERα mediate the differential effects of hyperoxia-induced damage in male and female OPCs.

Sunny Donna Elizabeth DE Hammer Elke E Strempel Sebastian S Joseph Christy C Manchanda Himanshu H Ittermann Till T Hübner Stephanie S Weiss Frank Ulrich FU Völker Uwe U Heckmann Matthias M

Molecular and cellular pediatrics 20200825 1

<h4>Background</h4>Hyperoxia is a well-known cause of cerebral white matter injury in preterm infants with male sex being an independent and critical risk factor for poor neurodevelopmental outcome. Sex is therefore being widely considered as one of the major decisive factors for prognosis and treatment of these infants. But unfortunately, we still lack a clear view of the molecular mechanisms that lead to such a profound difference. Hence, using mouse-derived primary oligodendrocyte progenitor ...[more]

PMID: 32844334

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Project description:Purpose: The aim of this study is (1) to identify the chromatin occupancy of the epigenetic regulator Smchd1 in neural stem cells (NSCs) derived from E14.5 mouse brain; (2) to profile key epigenetic marks H3K4me3, H3K27me3 and DNA methylation in wild type and Smchd1 null NSCs; (3) to identify the chromatin occupancy of Ctcf in wild type and Smchd1 null NSCs. Methods: Chromatin immunoprecipitation for Smchd1, H3K4me3, H3K27me3 and Ctcf was performed essentially as in (Nelson et al. 2006). Briefly, nuclei were isolated from formaldehyde crosslinked NSCs and chromatin was fragmented by sonication. Chromatin immunoprecipitation was performed with corresponding antibodies for Smchd1, H3K4me3 and H3K27me3. DNA was extracted from the immunoprecipitated fraction following reverse-crosslinking. Isolated DNA was used to generate sequencing libraries with Illumina's TruSeq DNA Sample Preparation Kit or Ovation Ultralow system (NuGen) according to manufacturer's instruction. Libraries were pooled and sequenced on the Illumina HiSeq 2000 platform for 100 bp single-end reads. Image analysis was performed in real time by the HiSeq Control Software (HCS) v1.4.8 and Real Time Analysis (RTA) v1.12.4.2, running on the instrument computer. Real-time base calling on the HiSeq instrument computer was performed with the RTA software. Illumina CASAVA1.8 pipeline was used to generate the sequence data. To examine the level of DNA methylation, genomic DNA was extracted using an AllPrep DNA/RNA Mini Kit (Qiagen) and methylated DNA was isolated via binding to the methyl-CpG binding domain of human MBD2 protein coupled beads using the MethylMiner methylated DNA enrichment kit (Life Technologies) according to the manufacturer’s instructions. Isolated DNA was used to generate sequencing libraries as for the ChIP-seq experiment with Illumina’s TruSeq DNA Sample Preparation Kit according to manufacturer's instruction and sequenced on the Illumina HiSeq 2000 platform for 49 bp single-end reads. Sequencing analysis was performed as described for the ChIP-seq experiments. Chromatin occupancy of the epigenetic regulator Smchd1 in neural stem cells (NSCs) derived from E14.5 mouse brain was determined by Smchd1 ChIP-seq. Enrichment of H3K4me3 and H3K27me3 in wild type and Smchd1 null NSCs were assessed by H3K4me3 and H3K27me3 ChIP-seq, respectively. DNA methylation in wild type and Smchd1 null NSCs was assessed by MBD-seq. Chromatin occupancy of Ctcf in wild type and Smchd1 null NSCs was determined by by Ctcf ChIP-seq.

Dataset Information

ChIP-Seq data from Nup133 ChIP performed on primary male and female mouse derived oligodendrocyte precursor cells

Publications

Nup133 and ERα mediate the differential effects of hyperoxia-induced damage in male and female OPCs.

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