Genome wide RNA-seq analysis of E14.5 Smchd1 wild type and mutant placenta
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Graham Kay
PROVIDER: E-GEOD-44668 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Shared Molecules
Only show the datasets with similarity scores above: 0.5
Threshold
0.5
Similar Datasets
Project description:We report the deregulation of expression in E9.5 male mouse embryos are that homozygous for a mutant allele of the Smchd1 gene (ie Smchd1MommeD1/MommeD1). RNA-seq analysis of Smchd1+/+ vs Smchd1MommeD1/MommeD1
2013-07-03 | E-GEOD-44665 | biostudies-arrayexpress
Project description:We report the deregulation of expression in Fi (C57Bl6/J x FVB/n) E14.5 male mouse placenta are that homozygous for a mutant allele of the Smchd1 gene (ie Smchd1MommeD1/MommeD1).
2013-07-03 | GSE44668 | GEO
Project description:Smchd1 appears to act as a tumour suppressor in the transformed fibroblast model. We find gene expression differences are most pronounced in the transformed MEFs. We always detect a small number of clustered genes and imprinted genes as differentially expressed, along with others involved in tumorigenesis. The microarrays compared Smchd1 null and Smchd1 wildtype samples from different cell types (primary MEFs, transformed MEFs, tumours derived from transformed MEFs). Wildtype mice are FVB/N and Smchd1 null mice have the MommeD1 point mutation on a FBV/N background.
2012-09-30 | E-GEOD-40734 | biostudies-arrayexpress
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.
2015-06-11 | E-GEOD-65748 | biostudies-arrayexpress
Project description:Using long-read nanopore sequencing, we obtained chromosome-wide phased methylomes of the active and inactive X in mouse placenta and neural stem cells (NSCs), overcoming the limitations if short-read bisulfite sequencing in allelic resolution. We also conducted quantitative analysis of methylation properties like symmetry and entropy, providing a more comprehensive view of epigenetic silencing in X chromosome inactivation. We also resolved the allele-specific genetics and epigenetics of structural macrosatellite Dxz4 and other repeats.
2024-03-12 | E-MTAB-13706 | biostudies-arrayexpress
Project description:Structural Maintenance of Chromosomes Hinge Domain Containing 1 (SMCHD1) is a chromatin repressor, which is mutated in >95% of Facioscapulohumeral dystrophy (FSHD) type 2 cases. In FSHD2, SMCHD1 mutations ultimately result in the presence of the cleavage stage transcription factor DUX4 in muscle cells due to a failure in epigenetic repression of the D4Z4 macrosatellite repeat on chromosome 4q, which contains the DUX4 locus. While binding of SMCHD1 to D4Z4 and its necessity to maintain a repressive D4Z4 chromatin structure are well documented, it is unclear how SMCHD1 is recruited to D4Z4, and how it exerts its repressive properties on the chromatin. Here, we employ a quantitative proteomics approach to identify and characterize novel SMCHD1 interacting proteins, and assess their functionality in D4Z4 repression. We identify 47 robust SMCHD1 interactors, of which 19 are present in D4Z4 chromatin. We demonstrate that one of these SMCHD1 interacting proteins in D4Z4, RuvB-like 1 (RUVBL1) is indeed required for maintaining DUX4 silencing in FSHD myocytes. We also confirm the interaction of SMCHD1 with EZH inhibitory protein (EZHIP), which prevents global H3K27me3 deposition by the Polycomb repressive complex PRC2, providing novel insights into the potential function of SMCHD1 in the repression of DUX4 in the early stages of embryogenesis. The SMCHD1 interactome outlined herein can thus provide further direction into research on the potential function of SMCHD1 at genomic loci where SMCHD1 is known to act, such as D4Z4 repeats, the inactive X chromosome, autosomal gene clusters, imprinted loci and telomeres.
2021-12-15 | PXD023993 | Pride
Project description:This SuperSeries is composed of the following subset Series: GSE40734: The effect on gene expression of Smchd1 deletion in primary MEFs, transformed MEFs and MEF tumours GSE40879: The effect on gene expression of Smchd1 deletion in pre-B cells from E17.5 Eµ-Myc embryos GSE40880: The effect on gene expression of Smchd1 deletion in end stage lymphomas GSE40881: The effect on gene expression of Smchd1 deletion in premalignant pre-B cells Refer to the individual subSeries. NOTE: all the cell types need to be analyzed separately.
2012-09-30 | E-GEOD-40992 | biostudies-arrayexpress
Project description:Here we show that Tet1 is down-regulated in mouse nucleus accumbens (NAc), a key brain reward structure, by repeated cocaine administration which enhances behavioral responses to cocaine. Through genome-wide 5hmC profiling, we identified 5hmC changes selectively clustered in both enhancer and coding regions of genes with several annotated neural functions. By coupling with mRNA sequencing, we found cocaine-induced alterations in 5hmC correlate positively with alternative splicing. We also demonstrated that 5hmC alteration at certain genes lasts up to a month after cocaine exposure. RNA Nac samples were collected at various time points after 7 daily cocaoine ip administration for 5hmC and transcriptome analysis
2015-02-23 | E-GEOD-63748 | biostudies-arrayexpress
Project description:Purpose: The aim of this study is to identify genes that are under the transcriptional control of the epigenetic regulator Smchd1 in neural stem cells (NSCs) derived from E14.5 mouse brain Methods: Total RNA was extracted using an AllPrep DNA/RNA Mini Kit (Qiagen) from cultured neural stem cells derived from male mouse E14.5 brains either wild-type or null for Smchd1. 1 µg total RNA was used to generate sequencing libraries for whole transcriptome analysis with Illumina’s TruSeq RNA Sample Preparation Kit v2 as per standard protocols. Libraries were sequenced on HiSeq 2000 with Illumina TruSeq SBS Kit v3-HS reagents as either 100 bp single-end or paired-end reads at the Australian Genome Research Facility (AGRF), Melbourne. Reads were aligned to the mouse reference genome mm10 and mapped to known genomic features at the gene level using the Rsubread package (version 1.10.5) (Liao et al. 2013). Mapped reads were then summarized into gene-level counts using FeatureCounts (Liao et al. 2014). Total RNA was extracted and purified from each cell line and their transcriptomes analyzed by RNA-Seq.
2015-06-11 | E-GEOD-65747 | biostudies-arrayexpress
Project description:Smchd1 appears to act as a tumour suppressor in the Eµ-Myc mouse B cell lymphoma model. We find a small number of gene expression differences at E17.5 in the pre-B cells, before phenotypic differences are observed. The microarrays compared Smchd1 null and Smchd1 wildtype E17.5 preB cell samples. All samples are on the C57BL/6 background and carry the Eµ-Myc transgene, and the Smchd1 null samples are additionally homozygous for a Smchd1 genetrap allele.
2012-09-30 | E-GEOD-40879 | biostudies-arrayexpress