RNAseq from disomic and trisomic T cells and monocytes
ABSTRACT: RNA was sequenced from Disomic and Trisomic individuals for chromosome 21 to identify consistent changes in gene expression across individuals Cells were cultured at subconfluency and RNA harvested for sequencing
Project description:RNA was sequenced from individuals Disomic and Trisomic for chromosome 21 to identify consistent changes in gene expression across individuals Cells were cultured at subconfluency and RNA harvested for sequencing
Project description:The function of a gene is closely connected to its expression specificity across tissues and cell types. RNA-Seq is a powerful quantitative tool to explore genome wide expression. The aim of the present study is to provide a comprehensive RNA-Seq dataset across the same 13 tissues for mouse and rat, two of the most relevant species for biomedical research. The dataset provides the transcriptome across tissues from three male C57BL6 mice and three male Han Wistar rats. We also describe our bioinformatics pipeline to process and technically validate the data. Principal component analysis shows that tissue samples from both species cluster similarly. By comparative genomics we show that many genes with high sequence identity with respect to their human orthologues have also a highly correlated tissue distribution profile and are in agreement with manually curated literature data for human. These results make us confident that the present study provides a unique resource for comparative genomics and will facilitate the analysis of tissue specificity and cross-species conservation in higher organisms.
Project description:Chronic early life stress increases adult susceptibility to numerous health problems linked to chronic inflammation. One way that this may occur is via glucocorticoid-induced developmental programming. To gain insight into such programming we treated zebrafish embryos with 1 micromolar cortisol and examined the effects on larvae. Treated larvae had elevated whole-body cortisol and glucocorticoid signaling, and up-regulated genes associated with defense response and immune system processes. 6 samples total were analyzed. 3 DMSO controls, and 3 cortisol treated (1 micromolar).
Project description:Chronic early life stress increases adult susceptibility to numerous health problems linked to chronic inflammation. One way that this may occur is via glucocorticoid-induced developmental programming. To gain insight into such programming, we treated zebrafish embryos with cortisol and examined the effects on adults. In adulthood, the treated fish maintained elevated basal cortisol levels in the absence of exogenous cortisol, and constitutively mis-expressed genes involved in defense response and its regulation. Adults derived from cortisol-treated embryos displayed defective tailfin regeneration, heightened basal expression of pro-inflammatory genes, and failure to appropriately regulate those genes following injury or immunological challenge. These results support the hypothesis that chronically elevated glucocorticoid signaling early in life directs development of a pro-inflammatory adult phenotype, at the expense of immunoregulation and somatic regenerative capacity. 30 samples total were analyzed. 9 caudal fins samples (0, 2 and 4dpa), 3 blood samples and 3 muscle samples from adults exposed to DMSO control as embryos. 9 caudal fins samples (0, 2 and 4dpa), 3 blood samples and 3 muscle samples from adults exposed to cortisol (1 micromolar) as embryos.
Project description:Dose-dependent hepatic gene expression was examined following repeated exposure (every 4 days for 28 days) to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). These data were used to examine the effect of repeated TCDD exposure as well as compare the performance of RNA-Seq and Agilent oligonucleotide microarrays for detection and identificatioin of differentially expressed genes. Five biological replicates for each dose (0.01, 0.03, 0.1, 0.3, 1, 3, 10, 30) of TCDD and sesame oil vehicle
Project description:Trisomy of chromosome 21, the genetic cause of Down syndrome, has the potential to alter expression of genes on chromosome 21, as well as other locations throughout the genome. These transcriptome changes are likely to underlie the Down syndrome clinical phenotypes. We have employed RNA-seq to undertake an in-depth analysis of transcriptome changes resulting from trisomy of chromosome 21, using induced pluripotent stem cells (iPSCs) derived from a single individual with Down syndrome. These cells were originally derived by Li et al, who genetically targeted chromosome 21 in trisomic iPSCs, allowing selection of disomic sibling iPSC clones. Analyses were conducted on trisomic/disomic cell pairs maintained as iPSCs or differentiated into cortical neuronal cultures. Overall design: 12 total polyA selected samples. 6 IPSC samples with 3 biological repeats for trisomic samples and 3 biological repeats for disomic samples. 6 IPSC derived neuronal samples with 3 biological repeats for trisomic samples and 3 biological repeats for disomic samples.
Project description:We used ATLAS-seq to map the sites of integration of an engineered LINE-1 (L1) retrotransposon into the genome of HeLa S3 cells. Then, we compared the position of these sites with publicly available genomic datasets. In order to cross-corroborate our findings with datasets obtained in the same cell stock as used in our retrotransposition assays, we also performed H3K4me1 ChIP-seq.
Project description:We used single cell RNA sequencing on 466 cells to capture the cellular complexity of the adult and fetal human brain at a whole transcriptome level. Healthy adult temporal lobe tissue was obtained from epileptic patients during temporal lobectomy for medically refractory seizures. We were able to classify individual cells into all of the major neuronal, glial, and vascular cell types in the brain. Examination of cell types in healthy human brain samples.
Project description:The inflammatory gene response requires activation of the protein kinase TAK1, but it is currently unknown how TAK1-derived signals coordinate transcriptional programs in the genome. We determined the genome-wide binding of the TAK1-controlled NF-κB subunit p65 in relation to active enhancers and promoters of transcribed genes by ChIP-seq experiments. Out of 35,000 active enhancer regions, 410 H3K4me1-positive enhancers show interleukin (IL)-1-induced H3K27ac and p65 binding. Inhibition of TAK1, IKK2 or depletion of p65 blocked inducible enhancer activation and gene expression. As exemplified by the CXC chemokine cluster located on chromosome 4, the TAK1-p65 pathway also regulates the recruitment kinetics of the histone acetyltransferase CBP, of NF-κB p50 and of AP-1 transcription factors to both, promoters and enhancers. This study provides a high resolution view of epigenetic changes occurring during the IL-1 response and allows the first genome-wide identification of a novel class of inducible p65 NF-κB-dependent enhancers in epithelial cells. ChIP-seq in KB cells with 5 different antibodies under different treatment conditions