Ontology highlight
ABSTRACT:
PROVIDER: PRJNA599152 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10834231_1.fastq.gz | Fastqsanger.gz | |||
| SRR10834231_2.fastq.gz | Fastqsanger.gz | |||
| SRR10834232_1.fastq.gz | Fastqsanger.gz | |||
| SRR10834232_2.fastq.gz | Fastqsanger.gz | |||
| SRR10834233_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 10 |
Similar Datasets
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare mouse NGS-derived oocyte、cumulus cell and blastocyst transcriptome profiling (RNA-seq) between PM2.5 exposure group and Filtrated air group Methods: mouse oocyte、cumulus cell and blastocyst mRNA profiles were generated by deep sequencing, in triplicate for each stage, using Illumina Hi-Seq 2500. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. Results: Using an optimized data analysis workflow, we mapped about 30 million sequence reads per sample to the mouse genome (build mm9). Genes with adjusted P < 0.05 and fold-change (FC) ≥ 2 were considered differentially expressed genes (DEGs). The oocyte transcriptome analysis showed that 467 DEGs (260 and 207 up- and down-regulated genes, respectively) were identified in the CAP group compared with the FA group. In the cumulus cell analysis, 592 DEGs (358 and 234 up- and down-regulated genes, respectively) were identified in the CAP group compared with the FA group. The blastocyst transcriptome analysis identified 448 DEGs (254 and 194 up- and down-regulated, respectively) in the CAP group compared with the FA group. Conclusions: Our study represents the first detailed analysis of mouse oocyte、cumulus cell and blastocyst transcriptomes, with biologic replicates, generated by RNA-seq technology between PM2.5 exposure group and Filtrated air group.
2020-04-14 | GSE148563 | GEO
Project description:Introduction: Prenatal and postnatal cigarette smoke exposure enhances the risk of developing asthma. Despite this as well as other smoking related risks, 11% of women still smoke during pregnancy. We hypothesized that cigarette smoke exposure during prenatal development generates long lasting differential methylation altering transcriptional activity that correlates with disease. Methods: In a house dust mite (HDM) model of allergic airway disease, we measured airway hyperresponsiveness (AHR) and airway inflammation between mice exposed prenatally to cigarette smoke (CS) or filtered air (FA). DNA methylation and gene expression were then measured in lung tissue. Results: We demonstrate that HDM-treated CS mice develop a more severe allergic airway disease compared to HDM-treated FA mice including increased AHR and airway inflammation. While DNA methylation changes between the two HDM-treated groups failed to reach genome-wide significance, 99 DMRs had an uncorrected p-value < 0.001. 6 of these 99 DMRs were selected for validation, based on the immune function of adjacent genes, and only 2 of the 6 DMRs confirmed the bisulfite sequencing data. Additionally, genes near these 6 DMRs (Lif, Il27ra, Tle4, Ptk7, Nfatc2, and Runx3) are differentially expressed between HDM-treated CS mice and HDM-treated FA mice. Conclusions: Our findings confirm that prenatal exposure to cigarette smoke is sufficient to modify allergic airway disease, however, it is unlikely that specific methylation changes account for the exposure-response relationship. These findings highlight the important role in utero cigarette smoke exposure plays in the development of allergic airway disease. Lung DNA methylation profiles of mice exposed in utero to cigarette smoke (CS) then treated with house dust mite (HDM, n = 8) or saline (n = 6), or exposed in utero to filtered air (FA) then treated with HDM (n = 9) or saline (n = 6)
2015-11-19 | E-GEOD-71718 | biostudies-arrayexpress
Project description:Homo sapiens isolate:NGS methods Genome sequencing
| PRJNA390232 | ENA
Project description:We study the role of loss of Setd2 and H3K36me3 in early B cell development through NGS methods including RNA, ChIP and ATAC Seq of sorted B cell populations of control and Setd2KO primary B cells from mice.
2020-03-23 | GSE130904 | GEO
Project description:Folic acid (FA) is well known to prevent neural tube defects (NTDs), but we do not know why many human NTD cases still remain refractory to FA supplementation. Here, we investigate how the DNA demethylase TET1 interacts with maternal FA status to regulate mouse embryonic brain development. We determined that cranial NTDs display higher penetrance in non-inbred than in inbred Tet1-/- embryos and are resistant to FA supplementation across strains. Maternal diets that are either too rich or deficient in FA are linked to an increased incidence of cranial deformities in wild type and Tet1+/- offspring and to altered DNA hypermethylation in Tet1-/- embryos, primarily at neurodevelopmental loci. Excess FA in Tet1-/- embryos results in phospholipid metabolite loss and reduced expression of multiple membrane solute carriers, including a FA transporter gene that exhibits increased promoter DNA methylation and thereby mimics FA deficiency. Moreover, FA deficiency reveals that Tet1 haploinsufficiency can contribute to DNA hypermethylation and susceptibility to NTDs. Overall, our study suggests that epigenetic dysregulation may underlie NTD development despite FA supplementation.
2024-11-08 | GSE276883 | GEO
Project description:Background: Although adequate periconceptional folic acid (FA) supplementation has reduced the occurrence of neural tube defects (NTDs)-affected pregnancies, mechanisms underlie FA resistant NTDs are poorly understood, so that NTDs still remain a global public health concern now. It has been proven that high level of Krüppel-like factor 12 (KLF12) has bad effects on heath in most cases, but there is no evidence concerning its roles during development. Methods: We used KLF12-overexpression mice to study the effects of high level of KLF12 on neural tube development. Findings: We showed KLF12-overexpression fetuses died in utero at around 10.5 days post coitus with 100% cranial NTDs. Neither FA or formate benefited normal neural tube closure in mutant fetuses. Further anylasis revealed high level of KLF12 caused NTDs in mice via overactivating Sonic hedgehog (Shh) signaling pathway, leading to upregulation of Ptch1, Gli1, Hhip etc. PF-5274857, an antagonist of Shh signaling pathway could significantly promote dorsolateral hinge point formation and partially rescue the phynotype. Interpretation: The regulatory hierarchy between high level of KLF12 and FA-resistant NTDs might provide new insights for the diagnosis and treatment of unexplained NTDs in the future.
2021-02-04 | GSE166054 | GEO
Project description:Neural tube defects (NTDs) are serious birth defects with an estimated worldwide incidence of 1 per 1,000 live births. The multifactorial nature of NTDs in humans has made it difficult to elucidate pathogenesis mechanisms. However, a strong relationship has been established between folate-homocysteine metabolism and NTD risk. Prevention of a substantial proportion of fetal NTDs can be achieved through maternal folic acid (FA) supplementation. However the mechanism by which FA exerts its beneficial effect remains unclear. METHODS: To improve our understanding of the underlying mechanisms of NTD pathogenesis and the ways in which folate exerts its beneficial effect, we analyzed mRNA profiles as well as folate and vitamin B12 levels in five NTD mouse mutants whose response to dietary FA was previously established. RESULTS: Differentially expressed genes representing the effect of each NTD-causing mutation were identified and associated with biologic pathways. Interestingly, the panel of NTD mutants collectively revealed pathways related to two nuclear receptors, retinoid X receptor (RXR) and pregnane X receptor (PXR), suggesting that these pathways may be related to a shared mechanism of NTD development. Moreover, the NTD-causing mutations that were associated with FA responsiveness had expression profiles that were related to folate-homocysteine metabolic pathways. These pathways were not strongly associated with mutants that do not respond to FA supplementation, implying that FA may be beneficial when the NTD mutation affects pathways related to folate-homocysteine metabolism. 5 groups of NTD mutants were studied. From each mutant group Heterozygous (test) and wild-type (control) female pups were used for this study at 6-8 weeks of age. 4 biological replicates were used for each of the test and control groups of each mutant. All mice used for the experiments were fasted 4-5 hours before dissection. A total of 36 samples were analyzed.
2013-09-30 | E-GEOD-51285 | biostudies-arrayexpress
Project description:To elucidate the transcriptional and epigenetic alterations underlying the neurogenic defects of FA-NSCs, we conducted gene expression microarray analysis and global DNA methylation profiling. The gene expression pattern of gene-corrected NSCs (C-FA-NSCs) resembled that of control-NSCs but clustered distantly from FA-NSCs (Fig. 6F and Table S1). Hierarchical clustering based on DNA methylation levels in the promoter region (+/-1.5kb from TSS) of genes whose expression levels were rescued in C-FA-NSCs, placed C-FA-NSCs closer to control-NSCs and away from FA-NSCs (Fig. 6G), although this pattern was not seen at the whole genome level (Fig. S4C). This suggests that FANCA gene correction leads to specific methylation changes in a subset of promoters. Examination of the methylomes of NSCs derived from Fanconi Anemia iPSCs before and after gene correction by targeted bisulfite sequencing with padlock probes
2014-05-15 | E-GEOD-57685 | biostudies-arrayexpress