CUT&Tag of H3K27me3, E9.5 Neural Tube defects mouse brain
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE299190 | GEO | 2025/12/30
REPOSITORIES: GEO
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Project description:To study the chromatin accessibility in E9.5d mouse brains with neural tube defects or control, we performed ATAC-seq in mouse brains. NTDs mouse model: CD-1 mice (7–8 weeks old) were provided by Beijing Vital River laboratory Animal Technology Co., Ltd, China (no: 110011200105514958, 16-25g). Female CD-1 mice were fed on low folate diet for more than 8 weeks. Sexually matured individuals were mated overnight; vaginal plug was detected at 8:00 am in the following morning and was designated as E0.5 day. NTDs mouse models were induced by intraperitoneal injection with 1.5 mg/kg of MTX (Sigma-Aldrich, USA) on E7.5. On E9.5, pregnant mice were euthanized by cervical dislocation, and the phenotypes of the fetuses were observed under a microscope. All samples with NTDs clinical manifestations were collected for experiments.
2025-12-30 | GSE299189 | GEO
Project description:This microarray study was conducted along with SATORI study, the clinical trial evaluated 125 patients with active RA with an inadequate response to low dose of MTX. Patients were allocated to receive either Tocilizumab(TCZ) 8 mg/kg every 4 weeks (TCZ group) or MTX 8 mg/week (MTX/control group) for 24 weeks. Gene expression profiles (GEP) of 112 patients - 54 patients from TCZ group and 58 patients from MTX group - were obtained in this study.
2014-01-29 | GSE35455 | GEO
Project description:<p>Maternal folic acid intake is crucial for the development of the offspring's nervous system, and folic acid metabolism disorders during pregnancy lead to neural tube defects (NTDs) in the fetus. Folic acid and vitamins biosynthesis is a major biochemical feature of gut microbiota. The complex and diverse microbial ecosystem residing within maternal host contributes critically to these intergenerational impacts. However, the mechanisms still require further investigation. In this study, we found that the low folate diets combined MTX-induced changed the structure/composition of the gut microbiota and substantially altered the fecal metabolic phenotype of pregnant mice, including central carbon metabolism in cancer and vitamin digestion & absorption. We demonstrated that the correlation betweent gut microbiota of pregnant mice and the brain metabolic profiles of NTDs fetal mice. According to our data, the Lactobacillales and Bifidobacteriales abundances in pregnant mice gut were positively correlated with the abundances of lipid metabolites in fetal mice brain. The abundances of Enterobacterales and Clostridiales were negatively correlated with those lipid metabolites. Interestingly, the abundance of Inosine, Uridine, L-Carnitine and Glycerophosphocholine were down-regulated synchronously in pregnant feces and NTDs fetal mice brain. This was probably the intergenerational microbial-metabolism biomarkers of NTDs. Our study provides evidence for how perinatal microecological factors shape fetal neural tube development.</p><p><br></p><p><strong>Feces metabolomics</strong> is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS4893' rel='noopener noreferrer' target='_blank'><strong>MTBLS4893</strong></a>.</p><p><strong>Brain tissue metabolomics</strong> is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS4894' rel='noopener noreferrer' target='_blank'><strong>MTBLS4894</strong></a>.</p>
2022-12-05 | MTBLS4893 | MetaboLights
Project description:Background: In the early stage of embryonic development, the neural tube (NT) cannot be closed properly due to some complex factors such as, environmental factors, genetic factors and the relationship between various factors, leading to the occurrence of neural tube defects (NTDs). Methods: In this study, we induced the mouse model of NTDs by feeding mice a low-folate diet and injecting 1.5mg/kg methotrexate on E7.5. Fetal mice were achieved at E13.5, then we extracted proteins from brain tissue with trypsin digestion. After enzymatic digestion, peptides were labeled with TMT/iTRAQ and then separated in high-performance liquid chromatography (HPLC) for subsequent LC-MS/MS analysis. To analyze the functional enrichment of differentially expressed proteins(DEPs) in the NTDs mice tissues with low folate induction, we used Gene Ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway annotation to analyze proteomic changes. Results: Low folate induced mouse model was successfully constructed. Folate was used as a sensitizing agent, the teratogenicity rate of the NTDs fetal mice was increased to 36.5% when methotrexate was injected to maternal mice at E7.5. 6614 proteins were identified by mass spectrometry, among them, 5656 proteins were quantified. In the following proteomic analysis, GO classification and KEGG pathway enrichment analysis were conducted, and heatmaps were drawn for differentially expressed proteins(DEPs). Moreover, the main pathways associated with NTDs, such as Hedgehog, Wnt, p53, Hippo signaling pathways, and one carbon pool by folate, can be identified through the generation of a protein-protein interaction (PPI) network. It was also found that the regulation of ribosomal proteins has a certain impact on neural tube development, such as RPL13 and RPL14, which are upregulated in NTDs. Conclusions: Our results revealed proteomic changes in the tissues of low folate induced NTDs mice, as well as validation showed that ribosomal proteins play a regulatory role during the development of NTDs, it provides new ideas for the pathogenesis and preventive measures of NTDs.
2024-03-12 | PXD045752 | Pride
Project description:Dimethylation of histone H3 lysine 9 (H3K9m2) and trimethylation of histone H3 lysine 27 (H3K27m3) are two hallmarks of transcriptional repression in many organisms. In Arabidopsis thaliana, H3K27m3 is targeted by Polycomb Group (PcG) proteins and is associated with silent protein coding genes, while H3K9m2 is correlated with DNA methylation and is associated with transposons and repetitive sequences. Recently, ectopic genic DNA methylation in the CHG context (where H is any base except G) has been observed in globally DNA hypomethylated mutants such as met1, but neither the nature of the hypermethylated loci nor the biological significance of this epigenetic phenomenon have been investigated. Here, we generated high-resolution genome-wide maps of both H3K9m2 and H3K27m3 in wild type and met1 plants, which we integrated with transcriptional data, to explore the relationships between these two marks. We found that most of the ectopic H3K9m2 observed in met1 is not due to defects in IBM1-mediated H3K9m2 demethylation, but instead targets H3K27m3-marked genes suggesting an interplay between these two silencing marks. Furthermore, H3K9m2/DNA-hypermethylation at these PcG targets in met1 is coupled with a decrease in H3K27m3 marks, whearas H3K9m2 hypomethylated transposons become ectopically H3K27me3 hypermethylated. Our results bear interesting similarities with cancer cells, which show global losses of DNA methylation, but ectopic hypermethylation of genes previously marked by H3K27m3. We used the met1-3 allele (Saze et al. 2003) and the salk_006042 line for isolating ibm1 mutants. met1-1st generation homozygous mutants and ibm1-1st generation homozygous mutants were isolated from a segragating population by genotyping. met1-2nd generation second mutants are the progeny of a single met1-1st generation homozygous mutant that was partially fertile. The entire shoots of 3 weeks old Arabidopsis plants (Col-0 ecotype), grown for 3 weeks under continuous light, were harvested, cross-linked as described in (Bernatavichute et al., 2007), frozen under liquid nitrogen and grown to powder (2g). Arabidopsis chromatin enriched for H3K9m2 and H3K27m3 was immunoprecipitated using an antibody that specifically recognizes H3K9m2 (Abcam 1220) and an antibody that specifically recognizes H3K27m3 (Upstate 07-449) respectively. Unmodified H3 was immunoprecipitated using Abcam 1791-100. Nucleosomal DNA and Input DNA were used as controls. ChIP, DNA purification and amplification were performed as in (Bernatavichute et al., 2007); Roche Nimblegen performed labelling and hybridization of the samples, washing and scanning resolution. All ChIP signals were normalized with either H3 ChIP or input genomic DNA by taking the log2 ratio and adjusted so that the average log2 ratio score across the genome was zero. 6 samples
2013-03-02 | E-GEOD-37075 | biostudies-arrayexpress
Project description:This microarray study was conducted along with SATORI study, the clinical trial evaluated 125 patients with active RA with an inadequate response to low dose of MTX. Patients were allocated to receive either Tocilizumab(TCZ) 8 mg/kg every 4 weeks (TCZ group) or MTX 8 mg/week (MTX/control group) for 24 weeks. Gene expression profiles (GEP) of 112 patients - 54 patients from TCZ group and 58 patients from MTX group - were obtained in this study. PB samples were collected directly into PAXGene tubes before and after the treatments. Total RNA was extracted using PAXGene Blood RNA Kit with the optimal on-column DNase digestion. Two-color microarray was used to directly compare the samples before versus after the treatment. Total RNA was amplified and amino allyl aRNA of the sample before/after treatments was further labeled with Cy3/Cy5. The labeled aRNAs (mixture of Cy3 and Cy5) was hybridized onto microarray slide. Dye swapping was done with each investigation to account for dye bias in microarray experiments.
2014-01-29 | E-GEOD-35455 | biostudies-arrayexpress
Project description:Dimethylation of histone H3 lysine 9 (H3K9m2) and trimethylation of histone H3 lysine 27 (H3K27m3) are two hallmarks of transcriptional repression in many organisms. In Arabidopsis thaliana, H3K27m3 is targeted by Polycomb Group (PcG) proteins and is associated with silent protein coding genes, while H3K9m2 is correlated with DNA methylation and is associated with transposons and repetitive sequences. Recently, ectopic genic DNA methylation in the CHG context (where H is any base except G) has been observed in globally DNA hypomethylated mutants such as met1, but neither the nature of the hypermethylated loci nor the biological significance of this epigenetic phenomenon have been investigated. Here, we generated high-resolution genome-wide maps of both H3K9m2 and H3K27m3 in wild type and met1 plants, which we integrated with transcriptional data, to explore the relationships between these two marks. We found that most of the ectopic H3K9m2 observed in met1 is not due to defects in IBM1-mediated H3K9m2 demethylation, but instead targets H3K27m3-marked genes suggesting an interplay between these two silencing marks. Furthermore, H3K9m2/DNA-hypermethylation at these PcG targets in met1 is coupled with a decrease in H3K27m3 marks, whearas H3K9m2 hypomethylated transposons become ectopically H3K27me3 hypermethylated. Our results bear interesting similarities with cancer cells, which show global losses of DNA methylation, but ectopic hypermethylation of genes previously marked by H3K27m3. Keywords: Genome binding/occupancy profiling by genome tiling array We used the met1-3 allele (Saze et al. 2003) and the salk_006042 line for isolating ibm1 mutants. met1-1st generation homozygous mutants and ibm1-1st generation homozygous mutants were isolated from a segragating population by genotyping. met1-2nd generation second mutants are the progeny of a single met1-1st generation homozygous mutant that was partially fertile. The entire shoots of 3 weeks old Arabidopsis plants (Col-0 ecotype), grown for 3 weeks under continuous light, were harvested, cross-linked as described in (Bernatavichute et al., 2007), frozen under liquid nitrogen and grown to powder (2g). Arabidopsis chromatin enriched for H3K9m2 and H3K27m3 was immunoprecipitated using an antibody that specifically recognizes H3K9m2 (Abcam 1220) and an antibody that specifically recognizes H3K27m3 (Upstate 07-449) respectively. Unmodified H3 was immunoprecipitated using Abcam 1791-100. Nucleosomal DNA and Input DNA were used as controls. ChIP, DNA purification and amplification were performed as in (Bernatavichute et al., 2007); Roche Nimblegen performed labelling and hybridization of the samples, washing and scanning resolution. All ChIP signals were normalized with either H3 ChIP or input genomic DNA by taking the log2 ratio and adjusted so that the average log2 ratio score across the genome was zero. 6 samples Processed data can be downloaded at http://danio.pellegrini.mcdb.ucla.edu/~hume/Deleris_PLoSGen2012_H3K9m2data.zip
2016-06-22 | E-GEOD-83606 | biostudies-arrayexpress
Project description:We sought to identify changes in placental gene expression that may contribute to the phenotype of NDRG1-deficient embryos, and to define the contribution of hypoxia and fetal sex to these changes. We therefore used high-density oligonucleotide microarrays to interrogate differences in placental gene expression, stratified by fetal sex, Ndrg1 status (WT vs KO) and oxygenation (21% vs 12%). C57Bl6/J mice heterozygous for NDRG1-null allele were bred and separated next day (E0.5), and give ad libitum access to standard chow and water with 12h light:dark cycle. Pregnant dams were sacrificed at E15.5 by cervical dislocation following isoflurane anesthesia. Following sacrifice, embryos and placentas were collected, NDRG1 genotype and sex were determined by PCR of fetal tissue, and RNA was extracted from placental tissue following removal of membranes.
2013-04-26 | E-GEOD-46381 | biostudies-arrayexpress
Project description:Neural tube defects (NTDs) are one of the most common human birth defects, with a prevalence of approximately 1 in 1000 live births in the United States. In animal studies, deletion of p53 and hyperthermia leads to a significant increase in embryos that exhibit exencephaly. To evaluate the effects of hyperthermia on p53-deficient mouse embryos we used microarray approach to find genes modified by deletion of p53 and hyperthermia treatment in day 8.5 mouse embryos to identify genes that may be involved in the mechanisms underlining NTDs and begin to define the developmental role of p53 in the etiology of NTDs.
2009-05-01 | GSE11547 | GEO
Project description:Neural tube defects (NTDs) are one of the most severe congenital abnormalities. Maternal folate deficiency could impact the occurrence of NTDs. Histone H3 methyltransferase disruptor of telomeric silencing 1-like (DOT1L) expression was significantly downregulated, and low levels of H3K79me2 were found in the corresponding NTDs samples with their maternal serum folate under low levels. Using ChIP-seq assays, we found that a decrease of H3K79me2 downregulates the expression of Shh and Sufu in mouse embryonic stem cells (mESC) under folate deficiency. Our results indicate that abnormal Shh and Sufu genes expression reduced by aberrant Dot1l-mediated H3K79me2 levels could be the cause of NTDs occurrence.
2023-07-25 | GSE238081 | GEO