High-throughput mapping of cellular differentiation hierarchies from single-cell data promises to empower systematic interrogations of vertebrate development and disease. Here, we applied single-cell RNA sequencing to >92,000 cells from zebrafish embryos during the first day of development. Using a graph-based approach, we mapped a cell state landscape that describes axis patterning, germ layer formation, and organogenesis. We tested how clonally related cells traverse this landscape by developing a transposon-based barcoding approach (“TracerSeq”) for reconstructing single-cell lineage histories. Clonally related cells were often restricted by the state landscape, including a case in which two independent lineages converge on similar fates. Cell fates remained restricted to this landscape in chordin-deficient embryos. We provide web-based resources for further analysis of the single-cell data. Overall design: Single-cell mRNA sequencing of zebrafish embryonic cells. Samples1-7: Single cell libraries from untreated embryos (4-24 hours post-fertilization). Samples8-12: Single cell libraries from embryos injected with TracerSeq lineage cassette at the 1-cell stage. Samples13-18: Single cell libraries from embryos injected with sgRNA + Cas9 at the 1-cell stage.
Single-cell mapping of gene expression landscapes and lineage in the zebrafish embryo.
Cell line, Treatment, Subject
View SamplesA number of breast or colon specific genes predictive of the relapse status were used in comparing the outcome from matched fresh frozen and stored in RNAlater preservative.
Prognostic gene expression signatures can be measured in tissues collected in RNAlater preservative.
No sample metadata fields
View SamplesOur aim is to identify circadian transcripts that are co-regulated with [Ca2+]cyt, with the eventual goal of identifying genetic regulators and targets for circadian oscillations of [Ca2+]cyt. We have identified two conditions in which [Ca2+]cyt behaves differently to other circadian outputs. 1. Treatment of plants with nicotinamide, a metabolic inhibitor of ADPR cyclase, abolishes the circadian oscillations of [Ca 2+]cyt. However, leaf movement, CCA1, LHY, TOC1 and CAB transcript abundance and CAB promoter activity are all rhythmic albeit with a longer period (Dodd et al., 2007). 2. The toc1-1 mutant, which shortens the circadian period of all other rhythms tested, has no effect on the period of [Ca2+]cyt oscillations (Xu et al., 2007). We will measure the circadian regulation of transcript abundance in wild type (C24), toc1-1 and nicotinamide (C24)-treated plants.
Correct biological timing in Arabidopsis requires multiple light-signaling pathways.
Specimen part, Treatment, Time
View SamplesHere we present the transcriptomic profile of mutant plants designated as ceh1 (constitutively expressing HPL). CEH1 encodes 1-hydroxy-2-methyl-2-butenyl 4-diphosphate synthase (HDS), the enzyme controlling the bottleneck step of the biosynthesis of isopentenyl diphosphate via the 2-C-methyl-d-erythritol-4-phosphate (MEP) pathway in the plastids. Mutation of this enzyme in ceh1 mutant led to accumulation of high levels of the stress specific signaling metabolite 2c-methyl-D-erythritol 2,4-cylclodiphosphate (MEcPP), and consequently constitutive activation of a selected otherwise stress responsive genes. This data identifies the ensemble of stress responsive genes whose expression is regulated by the MEcPP signaling cascade.
Plastid-produced interorgannellar stress signal MEcPP potentiates induction of the unfolded protein response in endoplasmic reticulum.
No sample metadata fields
View SamplesAn atlas of RNA and protein expression maps across a diverse set of developmental tissues from Zea mays Overall design: RNA-seq collected from a variety of maize tissues
Integration of omic networks in a developmental atlas of maize.
Specimen part, Subject
View SamplesFasting is the process of metabolic adaption to food deprivation that is taking place in most organisms, e.g. during the daily resting phase in mammals. Furthermore, in biomedical research fasting is used in most metabolic studies to synchronize nutritional states of study subjects. Because there is a lack of standardization for this procedure, we need a deeper understanding of the dynamics and the molecular players in fasting. In this study we investigated the transcriptome signature of white adipose tissue, liver, and skeletal muscle in 24 hours fasted mice (and chow fat controls) using Affymetrix whole-genome microarrays.
Metabolite and transcriptome analysis during fasting suggest a role for the p53-Ddit4 axis in major metabolic tissues.
Sex, Specimen part
View SamplesMammalian transcriptomes display complex circadian rhythms with multiple phases of gene expression that cannot be accounted for by current models of the molecular clock. We have determined the underlyingmechanisms by measuring nascent RNA transcription around the clock in mouse liver. Unbiased examination of eRNAs that cluster in specific circadian phasesidentified functional enhancers driven by distinct transcription factors (TFs). We further identify on a global scale the components of the TF cistromes that function to orchestrate circadian gene expression. Integrated genomicanalysesalso revealed novel mechanisms by which a single circadian factor controls opposing transcriptional phases. These findings shed new light on the diversity and specificity of TF function in the generation of multiple phases of circadian gene transcription in a mammalian organ.
Circadian enhancers coordinate multiple phases of rhythmic gene transcription in vivo.
Sex, Time
View SamplesWe generated a human EFTUD2 knockdown cell line using a CRISPR cas9 nickase strategy to investigate the effects of decreased expression of core spliceosome components on cell characteristics and global transcriptome expression/splicing patterns Overall design: 6 biological replicates of WT or CRISPR knock-down cells were generated and analysed by RNA-Seq
Disease modeling of core pre-mRNA splicing factor haploinsufficiency.
Cell line, Subject
View SamplesThe nuclear receptor PPAR gamma is required for adipocyte differentiation, but its role in mature adipocytes is less clear. Here we report that knockdown of PPAR gamma expression in 3T3-L1 adipocytes returned the expression of most adipocyte genes towards preadipocyte levels. Consistently, down regulated but not up regulated genes showed strong enrichment of PPAR gamma binding. Surprisingly, not all adipocyte genes were reversed and the adipocyte morphology was maintained for an extended period after PPAR gamma depletion. To explain this, we focused on transcriptional regulators whose adipogenic regulation was not reversed upon PPAR gamma depletion. We identified GATA2, a transcription factor whose down-regulation early in adipogenesis is required for preadipocyte differentiation, remaining low after PPAR gamma knockdown. Forced expression of GATA2 in mature adipocytes complemented PPAR gamma depletion and impaired adipocyte functionality with a more preadipocyte- like gene expression profile. Ectopic expression of GATA2 in adipose tissue in vivo had similar effect on adipogenic gene expression. These results suggest that PPAR gamma-independent down regulation of GATA2 prevents reversion of mature adipocytes after PPAR gamma depletion.
Re-expression of GATA2 cooperates with peroxisome proliferator-activated receptor-gamma depletion to revert the adipocyte phenotype.
No sample metadata fields
View SamplesThis dataset contains Affymetrix Mouse Genome 430 2.0 Array data obtained from K7M2 cells over-expressing ezrinT567A and the wild-type
Dysregulation of ezrin phosphorylation prevents metastasis and alters cellular metabolism in osteosarcoma.
Cell line
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