We compared transcriptional profiles of regenerating zebrafish caudal fins following fin amputation with profiles from uninjured zebrafish caudal fins Overall design: Examination of whole fin transcriptional profiles from regenerating fins (2 pools of 10 fins) and uninjured fins (2 pools of 10 fins)
Modulation of tissue repair by regeneration enhancer elements.
No sample metadata fields
View SamplesWe compared transcriptional and chromatin profiles of regenerating zebrafish hearts following genetic ablation with profiles from uninjured zebrafish hearts. Overall design: Examination of whole heart transcriptional profiles from ablated hearts (2 pools of 10 hearts) and uninjured hearts (2 pools of 10 hearts). Examination of differential H3K27Ac marks following genetic ablation of cardiomyocytes (regenerating hearts) and uninjured hearts.
Modulation of tissue repair by regeneration enhancer elements.
No sample metadata fields
View SamplesTo identify potential mRNA targets of FTO whose m6A levels are affected by FTO in acute myeloid leukemia (AML) cells, we conducted m6A-seq for messenger RNAs isolated from AML cells with and without forced expression of FTO. Overall design: We retrovirally transduced MSCV-PIG-FTO (i.e., human FTO) or MSCV-PIG (i.e., CTRL/Control) into human MONOMAC-6/t(9;11) AML cells and then selected individual stable clones under selection of puromuycin (0.5ug/ml). Four stable lines including two each FTO-overexpressing lines (i.e., FTO+ 1 and FTO+ 2; or FTO_1 and FTO_2) and control lines (i.e., WT 1 and WT 2; or Ctrl_1 and Ctrl_2) were selected for genome-wide m6A-sequencing (m6A-Seq) assays. The m6A-seq procedure was performed as detailed in Dominissini's method (Dominissini D., et al. Nat Protocols. 2013; 8: 176-189.). Polyadenylated RNA was extracted using FastTrack MAG Maxi mRNA isolation kit (Life technology). RNA fragmentation Reagents (Ambion) was used to randomly fragment RNA. M6A antibody (Synaptic Systems) was applied for m6A pull down. And final library preparation was constructed by TruSeq Stranded mRNA Sample Prep Kit (Illumina). Final library was quantified by BioAnalyzer High Sensitivity DNA chip then deeply sequenced on the Illumina HiSeq 2500.
FTO Plays an Oncogenic Role in Acute Myeloid Leukemia as a N<sup>6</sup>-Methyladenosine RNA Demethylase.
No sample metadata fields
View SamplesTo identify the expression of mRNAs after knockdown of FTO, we performed RNA-Seq in MA9.3ITD cells with or without knockdown of FTO. Overall design: We lentivirally transduced pLKO.1-shFTO (i.e., shFTO) or pLKO.1 empty vertor (i.e., shNS) into human MA9.3ITD (human CD34+ hematopoietic stem/progenetor cells stably infected by MLL-AF9 and FLT3-ITD) AML cells and then selected positively infected cells under selection of puromuycin (0.5ug/ml). The knockdown efficiency was confirmed by qPCR and western. Two stable lines including one FTO-knockdown cell line (i.e., shFTO) and one control line (i.e., shNS) were selected for RNA-Seq. Polyadenylated RNA was extracted using FastTrack MAG Maxi mRNA isolation kit (Life technology). RNA fragmentation Reagents (Ambion) was used to randomly fragment RNA. And final library preparation was constructed by TruSeq Stranded mRNA Sample Prep Kit (Illumina). Final library was quantified by BioAnalyzer High Sensitivity DNA chip then deeply sequenced on the Illumina HiSeq 2500.
FTO Plays an Oncogenic Role in Acute Myeloid Leukemia as a N<sup>6</sup>-Methyladenosine RNA Demethylase.
Specimen part, Cell line, Subject
View SamplesTo identify potential mRNA targets of FTO whose m6A levels are influenced in acute myeloid leukemia (AML) cells, we conducted m6A-seq for mRNA isolated from MA9.3ITD cells with and without knockdown of FTO Overall design: We lentivirally transduced pLKO.1-shFTO (i.e., shFTO) or pLKO.1 empty vertor (i.e., shNS) into human MA9.3ITD (human CD34+ hematopoietic stem/progenetor cells stably infected by MLL-AF9 and FLT3-ITD) AML cells and then selected positively infected cells under selection of puromuycin (0.5ug/ml). Two stable lines including one FTO-knockdown cell line (i.e., shFTO) and one control line (i.e., shNS) were selected for genome-wide m6A-sequencing (m6A-Seq) assays. The m6A-seq procedure was performed as detailed in Dominissini's method (Dominissini D., et al. Nat Protocols. 2013; 8: 176-189.). Polyadenylated RNA was extracted using FastTrack MAG Maxi mRNA isolation kit (Life technology). RNA fragmentation Reagents (Ambion) was used to randomly fragment RNA. M6A antibody (Synaptic Systems) was applied for m6A pull down. And final library preparation was constructed by TruSeq Stranded mRNA Sample Prep Kit (Illumina). Final library was quantified by BioAnalyzer High Sensitivity DNA chip then deeply sequenced on the Illumina HiSeq 2500.
FTO Plays an Oncogenic Role in Acute Myeloid Leukemia as a N<sup>6</sup>-Methyladenosine RNA Demethylase.
Specimen part, Subject
View SamplesTo evaluate the effect of IGF2BPs on mRNA stability and gene expression output, we conducted RNA-seq in individual IGF2BP knockdown and control HepG2 cells with or without actinomycin D treatment. Our RNA-seq and RNA stability profiling revealed that IGF2BPs were involved in RNA stability regulation and contributed to the stabilization of the transcriptome. Overall design: HepG2 cells were infected with individual lentiviral IGF2BP shRNA and non-specific control (shNS), and selected by puromycin to generate stable knockdown lines. We treated HepG2 cells with actinomycin D to inhibit transcription and collected cells at indicated time points (i.e., 0h, 1h, 3h, 6h). The total RNA was extracted by miRNeasy Kit (Qiagen) and sequenced by Illumina. For IGF2BP-dependent gene expression, untreated cells (i.e., 0h samples) were sequenced in triplicate and analyzed. For RNA stability profiling, RNA half-life was calculated by comparing the gene expression at 1, 3, 6 hours with actinomycin treatment to that in un-treated samples, with two biological replicates for each group.
Recognition of RNA N<sup>6</sup>-methyladenosine by IGF2BP proteins enhances mRNA stability and translation.
Specimen part, Treatment, Subject, Time
View SamplesWe used a reciprocal cross of Mus musculus and M. domesticus in which F1 males are sterile in one direction and fertile in the other direction, in order to associate expression differences with sterility.
Widespread over-expression of the X chromosome in sterile F₁hybrid mice.
Specimen part
View SamplesRNA-seq from R-2HG sensitive leukemia cells treated with R-2HG or PBS. Overall design: With MTT assays, we identified R-2HG exhibits an anti-leukemia function. We conducted RNA-Seq in the two sensitive cells (NOMO-1 and MA9.3ITD) with R-2HG or without R-2HG treatment for 48 hours to investigate which genes/a-ketoglutarate-dependent dioxygenases/signaling pathways are responsible for the anti-leukemia function of R-2HG. For each group, there are three duplicates.
R-2HG Exhibits Anti-tumor Activity by Targeting FTO/m<sup>6</sup>A/MYC/CEBPA Signaling.
Specimen part, Treatment, Subject
View SamplesA central challenge in pharmaceutical research is to investigate genetic variation in response to drugs. The Collaborative Cross (CC) mouse reference population is a promising model for pharmacogenomic studies because of its large amount of genetic variation, genetic reproducibility, and dense recombination sites. While the CC lines are phenotypically diverse, their genetic diversity in drug disposition processes, such as detoxification reactions, is still largely uncharacterized. Here we systematically measured RNA-sequencing expression profiles from livers of 29 CC lines under baseline conditions. We then leveraged a reference collection of metabolic biotransformation pathways to map potential relations between drugs and their underlying expression quantitative trait loci (eQTLs). By applying this approach on proximal eQTLs, including eQTLs acting on the overall expression of genes and on the expression of particular transcript isoforms, we were able to construct the organization of hepatic eQTL-drug connectivity across the CC population. The analysis revealed a substantial impact of genetic variation acting on drug biotransformation, allowed mapping of potential joint genetic effects in the context of individual drugs, and demonstrated crosstalk between drug metabolism and lipid metabolism. Our findings provide a resource for investigating drug disposition in the CC strains, and offer a new paradigm for integrating biotransformation reactions to corresponding variations in DNA sequences. Overall design: This dataset includes RNA-Seq data of mRNA that were extracted from the liver of 55 male mice. The 55 mice belong to 29 different collaborative cross strains. The number of individual mice per strains is 3 for 3 strains, 2 for 16 strains, and 1 for 8 strains. All the mice are naïve without any special treatment.
Dissecting the Effect of Genetic Variation on the Hepatic Expression of Drug Disposition Genes across the Collaborative Cross Mouse Strains.
Specimen part, Cell line, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The transcription factor GATA6 enables self-renewal of colon adenoma stem cells by repressing BMP gene expression.
Specimen part, Cell line
View Samples