This SuperSeries is composed of the SubSeries listed below.
Ha-ras and β-catenin oncoproteins orchestrate metabolic programs in mouse liver tumors.
Sex, Specimen part
View SamplesThe process of hepatocarcinogenesis in the diethylnitrosamine (DEN) initiation/phenobarbital (PB) promotion mouse model involves the selective clonal outgrowth of cells harboring oncogene mutations in Ha-ras, B-raf, or Ctnnb1. Here, we have characterized mouse liver tumors harboring either Ctnnb1 or Ha-ras mutations via integrated molecular profiling at the transcriptional and translational and post-translational levels. In addition, metabolites of the intermediary metabolism were quantified by high resultion 1H magic angle nuclear magnetic resonance (HR-MAS NMR). We have identified tumor characteristic genotype-specific differences in mRNA and miRNA expression, protein levels, and post-translational modifications and in metabolite levels that facilitate the molecular and biochemical stratification of tumor phenotypes. Bioinformatic integration of these data at the pathway level led to novel insights into tumor genotype-specific aberrant cell signaling and in particular to a better understanding of alterations in pathways of the cell intermediary metabolism, which are driven by the constitutive activation of the -Catenin and Ha-ras oncoproteins in tumors of the two genotypes.
Ha-ras and β-catenin oncoproteins orchestrate metabolic programs in mouse liver tumors.
Sex, Specimen part
View SamplesDeafness due to the terminal loss of inner ear hair cells is one of the most common sensory diseases. However, non-mammalian animals (e.g. birds, amphibian and fish) regenerate damaged hair cells. In order to better understand the reasons underpinning such regeneration disparities in vertebrates, we set out to define the changes in gene expression associated with the regeneration of hair cells in the zebrafish lateral line at high resolution. We performed RNA-Seq analyses on regenerating support cells purified by fluorescence activated cell sorting (FACS). The zebrafish lateral line provides an experimentally accessible system to define the complex signaling events triggered by injury and regeneration, because these cells can be acutely killed by exposure to neomycin, after which they regenerate rapidly. Lateral line hair cells are located in the center of a mechanosensory organ known as the neuromast and are surrounded by inner support cells and an outer ring of mantle cells. Tg(sqET20) larvae express GFP strongly in mantle cells and to a lesser degree in inner support cells. We isolated GFP positive and GFP negative cells from 5 days post fertilization (dpf) Tg(sqET20) larvae at 1, 3 and 5 hours post neomycin treatment, as well as from a non-treated control. Overall design: Transgenic zebrafish Tg(sqET20) larvae at 5 days post fertilization were exposed to neomycin, dissociated, and FACS sorted into GFP positive and GFP negative populations at 1, 3, and 5 hours following treatment, along with a mock treated 1 hr control. The experiment was performed in triplicate, for a total of 24 samples.
Gene-expression analysis of hair cell regeneration in the zebrafish lateral line.
No sample metadata fields
View SamplesThe goal of the experiments was to profile and analyze gene activity during murine pre-implantation development. Samples were collected at twelve time points from the germinal vesicle (GV) stage oocyte to the late (expanded) blastocyst.
A genome-wide study of gene activity reveals developmental signaling pathways in the preimplantation mouse embryo.
Age
View SamplesTranscriptomic profiling of breast cancer cells incubated in vitro with surgical wound fluids from patients with breast cancer reveals similarities in the biological response induced by intraoperative radiation therapy and the radiation-induced bystander effect
Surgical Wound Fluids from Patients with Breast Cancer Reveal Similarities in the Biological Response Induced by Intraoperative Radiation Therapy and the Radiation-Induced Bystander Effect-Transcriptomic Approach.
Specimen part, Cell line
View SamplesPurpose: To identify genes that are transcriptionally controlled by Notch signaling during zebrafish lateral line proneuromast formation. Methods: We isolated primordium cells from dissected tails of 36 hpf Tg((cldnB:GFP);Tg(cldnB:gal4) x Tg(UAS:nicd)) and sibling Tg((cldnB:GFP);Tg(cldnB:gal4)) embryos by FACS and performed RNASeq analysis. Results: Using an optimized data analysis workflow, we mapped about 26 million sequence reads per sample to the zebrafish genome (build danRer10) and identified 32,105 transcripts in the dissociated tails of WT and NICD zebrafish with TopHat workflow. Approximately 2% of the transcripts showed differential expression between the WT and NICD tails, with a fold change =0.5 and p value <0.01. Conclusion: RNASeq analyses revealed that Notch signaling cell-autonomously induces apical constriction and cell adhesion. Overall design: Zebrafish lateral line mRNA profiles of 36 hours wild type (WT) and NICD embryos were generated in triplicate, using HiSeq 2500 (Illumina).
Proliferation-independent regulation of organ size by Fgf/Notch signaling.
No sample metadata fields
View SamplesThe transmission of information about the photic environment to the circadian clock involves a complex array of neurotransmitters, receptors, and second messenger systems. Using laser capture microscopy and microarray analysis, a population of genes rapidly induced by light in the suprachiasmatic nucleus is identified.
Identification of novel light-induced genes in the suprachiasmatic nucleus.
No sample metadata fields
View SamplesT lymphocytes are essential contributors to the adaptive immune system and consist of multiple lineages that serve various effector and regulatory roles. As such, precise control of gene expression is essential to the proper development and function of these cells. Previously, we identified Snai2 and Snai3 as being essential regulators of immune tolerance partly due to the impaired function of CD4+ regulatory T cells in Snai2/3 conditional double knockout mice. Here we extend those previous findings using a bone marrow transplantation model to provide an environmentally unbiased view of the molecular changes imparted onto various T lymphocyte populations once Snai2 and Snai3 are deleted. The data presented here demonstrate that Snai2 and Snai3 transcriptionally regulate the cellular fitness and functionality of not only CD4+ regulatory T cells but effector CD8a+ and CD4+ conventional T cells as well. This is achieved through the modulation of gene sets unique to each cell type and includes transcriptional targets relevant to the survival and function of each T cell lineage. As such, Snai2 and Snai3 are essential regulators of T cell immunobiology. Overall design: GFP- CD3e+ CD8a+ CD4-, GFP- CD3e+ CD8a- CD4+ CD25- and GFP- CD3e+ CD8a- CD4+ CD25+ T cells were isolated from spleens of UBC-GFP mice transplanted with WT or cDKO lineage-depleted donor bone marrow following lethal irradiation of recipient mice. RNA-seq was performed on 3-4 biological replicates from each genotype for all T cell populations analyzed.
Snai2 and Snai3 transcriptionally regulate cellular fitness and functionality of T cell lineages through distinct gene programs.
Specimen part, Cell line, Subject
View SamplesThe prostate represents a complex mix of cell types and there is a need to analyze distinct cell populations to better understand their potential interactions. This study of cell-type specific gene expression patterns will contribute to understanding of how tumor epithelial cells may be affected by adjacent interstitial stromal cells within the tumor microenvirnonment.
Analysis of gene expression in prostate cancer epithelial and interstitial stromal cells using laser capture microdissection.
Specimen part, Disease, Disease stage
View SamplesPrimary murine hepatocytes were transfected with siRNA targeting Caveolin-1 directly after attachment (o/n). Next day, cells were treated with TGF-beta for 48 h. Experiment was performed in triplicate using primary cells from 3 donor mice.
Caveolin-1 Impacts on TGF-β Regulation of Metabolic Gene Signatures in Hepatocytes.
Treatment
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