We compare whole-animal RNA-seq transcriptomes for C. elegans males and hermaphrodites from the late L3 larval stage to young adulthood. During this interval, male sexual structures develop, including extensive neurogenesis and synaptogenesis that nearly doubles the size of the nervous system. Previous genome-wide expression studies in C. elegans have usually focused on only one sex – the hermaphrodite, and there are a relatively large number of predicted genes that still remain without meaningful annotation. In the present study, differential expression analysis of the RNA-seq data revealed 1,751 genes expressed at a higher level in the male. By differential expression analysis, unbiased gene correlation analysis, and a guilt-by-association approach, we identified new transcription factors required for differentiation of male genital structures, semen proteins, and candidates for previously-unknown components for synapse function. The results validate the dataset as a rich resource for future gene discovery in C. elegans. Overall design: To analyze gene expression during sexual maturation in C. elegans, we performed RNA-seq for five samples for each sex ranging at 6 hr intervals from late L3 to young adult stages
Gene Function Prediction Based on Developmental Transcriptomes of the Two Sexes in C. elegans.
Sex, Subject, Time
View SamplesGene expression profiling was carried out on peripheral blood mononuclear cell mRNA samples collected from 4 mo old rhesus macaques subject to maternal rearing, peer rearing, or surrogate peer rearing. The primary research question is whether gene expression differs as a function of early rearing conditions.
Transcriptional modulation of the developing immune system by early life social adversity.
Age
View SamplesHypoxia promotes an aggressive tumor phenotype with increased genomic instability, partially due to downregulation of DNA repair pathways. However, in addition to DNA repair, genome stability is also controlled by cell cycle checkpoints. An important issue is therefore whether hypoxia also can alter the DNA damage cell cycle checkpoints. Here, we show that hypoxia (24h 0.2% O2) alters the expression of several G2 checkpoint regulators, as examined by microarray gene expression analysis and immunoblotting of U2OS cells. While some of the changes reflected hypoxia-induced inhibition of cell cycle progression, flow cytometric bar-coding analysis of individual cells showed that the levels of several G2 checkpoint regulators were reduced in G2 phase cells after hypoxic exposure, in particular cyclin B1. These effects were accompanied by decreased Cyclin dependent kinase (CDK) activity in G2 phase cells after hypoxia. Furthermore, cells pre-exposed to hypoxia showed a longer G2 checkpoint arrest upon treatment with ionizing radiation. Similar results were found following other hypoxic conditions (~0.03 % O2 20h and 0.2% O2 72h). These results demonstrate that the DNA damage G2 checkpoint can be altered as a consequence of hypoxia, and we propose that such alterations may influence the genome stability of hypoxic tumors.
Hypoxia-induced alterations of G2 checkpoint regulators.
Specimen part, Cell line
View SamplesThe level of trypsin-2 has been shown to correlate with the malignancy and metastatic potential of many cancer.
Trypsin-2 enhances carcinoma invasion by processing tight junctions and activating ProMT1-MMP.
Specimen part, Cell line
View SamplesMaintaining metabolic homeostasis in response to fluctuating nutrient intake requires intricate coordination between tissues of multicellular animals. The insulin/glucagon axis is well known to hormonally coordinate organism-wide carbohydrate metabolism. The ChREBP/Mondo-Mlx transcription factors regulate glycolytic and lipogenic genes locally in hepatocytes and adipocytes, but its role in systemic metabolic homeostasis has remained poorly understood. We demonstrate that Mondo-Mlx controls gene activity in several peripheral tissues of Drosophila melanogaster, where it regulates nutrient digestion and transport as well as carbohydrate, amino acid and lipid metabolism. In addition to directly regulating metabolic genes Mondo-Mlx controls a regulatory network composed of the Activin ligand Dawdle and GLI similar transcription factor Sugarbabe. Dawdle and Sugarbabe contribute to the regulation of a subset of Mondo-Mlx-dependent processes, including sugar-induced de novo synthesis of serine and fatty acids. In summary, our study establishes Mondo-Mlx sugar sensor as a master regulator of organismal metabolic homeostasis upon sugar feeding. Overall design: Control (sug17d/+) and sugarbabe null mutant (sug17d/sug def) third instar larvae were fed control low sugar or high sugar diet and total RNA was extracted from the whole larvae.
Mondo-Mlx Mediates Organismal Sugar Sensing through the Gli-Similar Transcription Factor Sugarbabe.
Specimen part, Subject
View SamplesTo decode the complexed mechanism controlling HSC expansion, from the viewpoint of systems biology, we performed spatial transcriptome analysis by dissecting the whole hematopoietic organ, CHT. Overall design: All the reagents and instruments used in this experiment are RNase-free. The fresh 52 hpf zebrafish tail was embedded in OCT with vertical position and rapid frozen in liquid nitrogen. The cryosection was stained with cresyl violet before laser microdissection. Each sample of sections was acquired using specific LCM platforms. The tail region of 52 hpf zebrafish embryo was cut for cryo-section and six sets of samples (including neuro (N), left muscle (L), right muscle (R), caudal artery (CA), caudal vein (CV) and caudal vein plexus (CVP)) were harvested from each section by Laser Capture Microdissection (LCM).
A 3D Atlas of Hematopoietic Stem and Progenitor Cell Expansion by Multi-dimensional RNA-Seq Analysis.
Specimen part, Subject
View SamplesReliable identification of cancer markers can have substantial implications to early detection of cancer. We report here an integrated computational and experimental study on identification of gastric cancer markers in patients tissue and sera based on (i) genome-scale transcriptomic analyses on 80 paired gastric cancer/reference tissues, with the aim of identifying abnormally expressed genes at various subtypes/stages of gastric carcinoma (ii) a computational identification of differentially expressed genes that may have their proteins secreted into blood circulation, followed by experimental validations.
An integrated transcriptomic and computational analysis for biomarker identification in gastric cancer.
Sex, Age, Specimen part, Disease stage
View SamplesDM1 and DM2 biopsies from patients were compared to Normal adult individuals
Differences in aberrant expression and splicing of sarcomeric proteins in the myotonic dystrophies DM1 and DM2.
No sample metadata fields
View SamplesThe composition of the matrix molecules is important in in vitro cell culture experiments of e.g. human cancer invasion and vessel formation. Currently, the mouse Engelbreth-Holm-Swarm (EHS) sarcoma -derived products, such as Matrigel, are the most commonly used tumor microenvironment mimicking (TMEM) matrices for experimental studies. However, since Matrigel is non-human in origin, its molecular composition does not accurately simulate human TMEM and we expect myogel to be more natural environment for human cancer cells. The environment may have crucial impact on cell behavior and gene expression.
A novel human leiomyoma tissue derived matrix for cell culture studies.
Cell line
View SamplesWe analyzed chromatin dynamics and transcriptional activity of human embryonic stem cell (hESC)-derived cardiac progenitor cells (CPCs) and KDR+/CD34+ endothelial cells generated from cardiogenic or hemogenic mesoderm. Using an unbiased algorithm to hierarchically rank genes modulated at the level of chromatin and transcription, we identified novel candidate regulators of mesodermal lineage determination. HOPX, a non-DNA binding homeodomain protein, was identified as a candidate regulator of blood-forming endothelial cells. We used HOPX reporter and knockout hESCs, as well as hopx loss of function studies in zebrafish, to show the requirement of HOPX in vivo and in vitro in hemato-endothelial lineage specification. Loss of HOPX does not impact endothelial fate specification but markedly reduces primitive hematopoiesis acting at least in part through suppression of Wnt/ß-catenin signaling. Single cell RNA-seq data during mouse hematopoietic development in vivo confirm a role for HOPX in hematopoietic fate. Taken together, we show that HOPX is a novel regulator of hemato-endothelial fate specification in vitro and in vivo that functionally regulates Wnt signaling to modulate primitive hematopoiesis. Overall design: 2 biological replicates were isolated from cardiac progenitor cells (CPCs) and endothelial populations derived from cardiogenic mesoderm (C-ECs) and hemogenic mesoderm (H-ECs). RNA-seq and ChIP-seq (H3K4me3 and H3K27me3) was performed for each replicate.
Single-Cell Transcriptomic Analysis of Cardiac Differentiation from Human PSCs Reveals HOPX-Dependent Cardiomyocyte Maturation.
No sample metadata fields
View Samples