Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mouse whole brain: Alteration of DNA methylation status caused by prenatal titanium dioxide nanoparticle exposure

ABSTRACT: Reportedly, titanium dioxide nanoparticle exposure during pregnancy can affect the development of the central nervous system in mouse offspring; however, the underlying mechanism remains unknown. In the present study, we investigated the impact of prenatal dioxide nanoparticle exposure on global DNA methylation in the brains of neonatal mice. Pregnant C57BL/6J mice were intratracheally administered a dioxide nanoparticle suspension (100 ug/mouse) on gestational day 10.5, and brains were collected from male and female offspring at day 1 postpartum. After extraction of methylated DNA by immunoprecipitation, the DNA methylation profile was analyzed using a mouse CpG island microarray. Among genes in the CpG island microarray, DNA methylation was increased in 614 and 2924 genes and decreased in 6219 and 6463 genes in male and female offspring, respectively. Combined with mRNA microarray analysis, 88 and 89 genes were upregulated (≥ 1.5-fold) accompanied by demethylation of CpG islands, whereas 13 and 33 genes were downregulated (≤ 0.67-fold) accompanied by demethylation of CpG islands in male and female offspring mice, respectively. Gene Set Enrichment Analysis (GSEA) revealed that these genes were enriched in gene ontology terms related to the regulation of transcription factors, cell proliferation, and organism development. Additionally, MeSH terms related to stem cells and morphogenesis were enriched.

ORGANISM(S): Mus musculus

PROVIDER: GSE178202 | GEO | 2021/10/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Mouse whole brain: Alteration of gene expression caused by prenatal titanium dioxide nanoparticle exposure

Project description:Reportedly, titanium dioxide nanoparticle exposure during pregnancy can affect the development of the central nervous system in mouse offspring; however, the underlying mechanism remains unknown. We investigated the impact of prenatal dioxide nanoparticle exposure on mRNA expression patterns in the brains of neonatal mice. Pregnant C57BL/6J mice were intratracheally administered a dioxide nanoparticle suspension (100 ug/mouse) on gestational day 10.5, and brains were collected from male and female offspring at day 1 postpartum. Total RNA was obtained, and mRNA expression profiles were comprehensively assessed using microarray analysis. The results showed 88 and 89 genes were upregulated (≥ 1.5-fold) accompanied by demethylation of CpG islands, whereas 13 and 33 genes were downregulated (≤ 0.67-fold) accompanied by demethylation of CpG islands in male and female offspring mice, respectively. Gene Set Enrichment Analysis (GSEA) revealed that these genes were enriched in gene ontology terms related to the regulation of transcription factors, cell proliferation, and organism development. Additionally, MeSH terms related to stem cells and morphogenesis were enriched.

2021-10-04 | GSE178199 | GEO

E2F6 initiates stable epigenetic silencing of germline genes during embryonic development

Project description:In mouse development, long-term silencing by CpG island DNA methylation is specifically targeted to germline genes, however the molecular mechanisms of this specificity remain unclear. Here we demonstrate that the transcription factor E2F6, a member of the polycomb repressive complex 1.6 (PRC1.6), is critical to target and initiate epigenetic silencing at germline genes in early embryogenesis. Genome-wide, E2F6 binds preferentially to CpG islands in embryonic cells. E2F6 cooperates with MGA to silence a subgroup of germline genes in mouse embryonic stem cells and in vivo, a function that critically depends on the E2F6 marked box domain. Inactivation of E2f6 leads to a failure to deposit CpG island DNA methylation at these genes during implantation. Furthermore, E2F6 is required to initiate epigenetic silencing in early embryonic cells but becomes dispensable for the maintenance in differentiated cells. Our findings elucidate the mechanisms of epigenetic targeting of germline genes and provide a paradigm for how transient repression signals by DNA-binding factors in early embryonic cells are translated into long term epigenetic silencing during mammalian development.

2021-04-22 | PXD023974 | Pride

Comparison of DNA methylation profiles in diploid and transformed tetraploid MEF cells

Project description:We propose that tetraploidy induces epigentic changes including DNA methylation due to the abnormal chromatin in the cells. To test our hypothesis, we employed methylated CpG island recovery assay (MIRA) assisted microarray to determine the DNA methylation profiles in both diploid and tetraploid cells. First, we conducted a methylated-CpG island recovery assay (MIRA). Briefly, we enriched for methylated CpG islands with methylated DNA binding proteins, MBD2/MBD3L1. The pulled down DNA fragments containing CpG islands and input DNA fragments were amplified with real-time PCR. After labeling, they were hybridized to CpG island promoter array. Data were collected and analyzed.

2012-04-29 | E-GEOD-18814 | biostudies-arrayexpress

DNA hypermethylation encroachment at CpG island borders in cancer is predisposed by H3K4 monomethylation [WGBS_Hs]

Project description:DNA methylation plays a key role in demarcation of regulatory regions, including promoter-associated CpG islands. While CpG islands are typically maintained in an unmethylated state in normal cells, a proportion of CpG islands are subject to hypermethylation in cancer cells. It still remains elusive how the exquisite demarcation of the bimodal methylation state is established and maintained at the CpG island flanks and conversely what triggers the erosion of CpG island DNA methylation in tumorigenesis. Here, we applied whole-genome bisulphite sequencing to study the comprehensive methylation patterns of prostate normal and cancer tissues. Alongside we performed TET-assisted bisulphite sequencing to study genome-wide DNA hydroxymethylation patterns of normal prostate and prostate cancer tissues.

2019-01-23 | GSE104789 | GEO

DNA hypermethylation encroachment at CpG island borders in cancer is predisposed by H3K4 monomethylation [TAB-Seq]

2019-01-23 | GSE104780 | GEO

KDM2B binds CpG islands and modulates recruitment of Ring1b

Project description:CpG island elements are associated with most mammalian gene promoters, yet how they contribute to gene regulation remains poorly understood. Recently it has become clear that a subset of CpG islands in embryonic stem cells can act as polycomb response elements and are recognized by the polycomb silencing systems to regulate the expression of genes involved in pluripotency and early developmental transcription programs. How CpG islands function mechanistically as nucleation sites for polycomb repressive complexes remains unknown. Here we discover that the KDM2B protein, by virtue of its ZF-CxxC DNA binding domain, specifically recognizes non-methylated DNA in CpG islands elements genome-wide. Through a physical interaction with the polycomb repressive complex 1 (PRC1), KDM2B targets PRC1 to CpG islands where it contributes to H2AK119ub1 and gene repression at a subset of polycomb targets. Unexpectedly, we also find that CpG islands are occupied by low levels of PRC1 throughout the genome, suggesting that the KDM2B-PRC1 complex may sample CpG island associated genes for susceptibility to polycomb mediated silencing. These observations demonstrate an unexpected and direct link between recognition of CpG islands by KDM2B and targeting of the polycomb repressive system. This provides the basis for a new model describing the functionality of CpG islands as mammalian PREs.

2012-12-26 | GSE40860 | GEO

BANP opens chromatin and activates CpG island regulated genes [ATAC-Seq]

Project description:In mammalian genomes, the vast majority of RNA polymerase II initiation events take place at CpG island promoters. Despite their relevance our understanding of their regulation remains limited. Here we identify Banp as the long sought-after TF that binds the orphan CGCG element in CpG islands by combining single-molecule footprinting with interaction proteomics. We show that Banp drives activity of CpG islands that control essential metabolic genes in the mouse and human genome. Banp binding is strongly repelled by DNA methylation of its motif in vitro and in vivo, which restricts most binding to CpG islands and accounts for its absence at aberrantly methylated CpG islands in cancer cells. Upon binding to an unmethylated motif, Banp opens chromatin and positions nucleosomes. These findings expand our understanding of CpG island gene regulation and put forth a model whereby CpG islands rely for their activity on methylation sensitive TFs capable of opening and organizing chromatin.

2021-05-17 | GSE155601 | GEO

BANP opens chromatin and activates CpG island regulated genes [MNase-seq]

2021-05-17 | GSE155600 | GEO

BANP opens chromatin and activates CpG island regulated genes [RNA-Seq]

2021-05-17 | GSE155664 | GEO

BANP opens chromatin and activates CpG island regulated genes [ChIP-Seq]

2021-05-17 | GSE155603 | GEO