Filters
Technology
Platform
SRP144405
Mus musculus
34 Downloadable Samples
Illumina HiSeq 1500
Description
In mammals, chromosomes are partitioned into megabase-sized topologically associating domains (TADs). TADs can be in either A (active) or B (inactive) subnuclear compartments, which correspond to early (E) and late (L) replicating timing (RT) domains, respectively. Here, we show that RT changes are tightly correlated with A/B compartment changes during mouse embryonic stem cell (mESC) differentiation. A/B compartments changed mostly by a “boundary shift,” frequently causing compartment switching of single TADs, which coincided with or preceded RT changes. Upon differentiation, mESCs acquired an A/B compartment organization that closely resembled EpiSCs (epiblast-derived stem cells), suggesting that accumulation of compartment boundary repositioning eventually led to naïve-to-primed pluripotency transition in A/B compartment organization. We propose that large-scale reorganization of A/B compartments, which is reflected in RT domain reorganization, represents major cell fate changes. Collectively, our data provides valuable insights into the regulatory principles of 3-dimensional (3D) genome organization during early embryonic stages. Overall design: RNA-Seq: 9 cell types, with a total of 34 individual replicates.
Publication Title
Single-cell DNA replication profiling identifies spatiotemporal developmental dynamics of chromosome organization.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 5 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Metabolism is tightly coupled with the process of aging, and tumorigenesis. However, the mechanisms regulating metabolic properties in different contexts remain unclear. Cellular senescence is widely recognized as an important tumor suppressor function and accompanies metabolic remodeling characterized by increased mitochondrial oxidative phosphorylation (OXPHOS). Here we showed retinoblastoma (RB) is required for the increased OXPHOS in oncogene-induced senescent (OIS) cells. Combined metabolic and gene expression profiling revealed that RB mediated activation of the glycolytic pathway in OIS cells, causing upregulation of several glycolytic genes and concomitant increases in the levels of associated metabolites in the glycolytic pathway. Knockdown of these genes by small interfering RNAs (siRNAs) resulted in decreased mitochondrial respiration, suggesting that RB-mediated glycolytic gene activation promotes metabolic flux into the OXPHOS pathway. These results suggest that coordinate transcriptional activation of metabolic genes by RB enables OIS cells to maintain metabolically bivalent states that both glycolysis and OXPHOS are highly active. Collectively, our findings demonstrated a previously unrecognized function of RB in OIS cells.
Publication Title
Retinoblastoma protein promotes oxidative phosphorylation through upregulation of glycolytic genes in oncogene-induced senescent cells.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 3 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
By transcriptome analysis of IMR-90 human fibroblasts following oncogene-induced senescence (OIS) and replicative senescence (RS), we identified commonly regulated genes in both conditions.
Publication Title
The SETD8/PR-Set7 Methyltransferase Functions as a Barrier to Prevent Senescence-Associated Metabolic Remodeling.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 3 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Cellular senescence is an ireversible growth arrest with alterd metabolic potentials including DNA, RNA and protein dynamics. We found that loss of the SETD8/PR-Set7 methyltransferase, which catalyzes mono-methylation of histone H4 at lysine 20 (H4K20me1), induces senescence in human fibroblasts. To investigate the role of SETD8 in cellular senescence, we performed a microarray-based transcriptomic analysis in SETD8-knockdown cells. Our results demonstrate that SETD8 links the epigenomic gene regulation to senescence-associated metabolic remodeling.
Publication Title
The SETD8/PR-Set7 Methyltransferase Functions as a Barrier to Prevent Senescence-Associated Metabolic Remodeling.
Sample Metadata Fields
Cell line
View Samples- Arabidopsis thaliana
- 17 Downloadable Samples
- Illumina HiSeq 2000
Description
Wounding is a primary trigger of organ regeneration but how wound stress reactivates cell proliferation and promotes cellular reprogramming remains elusive. In this study we combined the transcriptome analysis with quantitative hormonal analysis to investigate how wounding induces callus formation in Arabidopsis thaliana. Our time-course RNA-seq analysis revealed that wounding induces dynamic transcriptional changes that can be categorized into five clusters with distinct temporal patterns. Gene ontology analyses uncovered that wounding modifies the expression of hormone biosynthesis and response genes, and quantitative analysis of endogenous plant hormones revealed accumulation of cytokinin prior to callus formation. Mutants defective in cytokinin synthesis and signalling display reduced efficiency in callus formation, indicating that de novo synthesis of cytokinin has major contribution in wound-induced callus formation. We further demonstrate that type-A ARABIDOPSIS RESPONSE REGULATOR (ARR)-mediated cytokinin signalling regulates the expression of CYCLIN D3;1 (CYCD3;1) and mutations in CYCD3;1 and its homologs CYCD3;2-3 cause defects in callus formation. Our transcriptome data, in addition, showed that wounding activates multiple developmental regulators, and we found novel roles of ETHYLENE RESPONSE FACTOR 115 (ERF115) and PLETHORA3 (PLT3), PLT5, PLT7 in wound-induced callus formation. Together, this study provides novel mechanistic insights into how wounding reactivates cell proliferation during callus formation. Overall design: Examination of transcriptome at 0, 1, 3, 6, 12,24 h after wounding.
Publication Title
Wounding Triggers Callus Formation via Dynamic Hormonal and Transcriptional Changes.
Sample Metadata Fields
Specimen part, Subject, Time
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Thalamocortical axons pass through the prethalamus in the first step of their neural circuit formation Although it has been supposed that the prethalamus is an intermediate target for thalamocortical projection formation, much less is known about the molecular mechanisms of this targeting.
Publication Title
Development of the prethalamus is crucial for thalamocortical projection formation and is regulated by Olig2.
Sample Metadata Fields
Specimen part
View Samples- Gallus gallus
- 2 Downloadable Samples
- Affymetrix Chicken Genome Array (chicken)
Description
PTIP (Pax2 transactivation domain-interacting protein) is a nuclear protein containing six BRCT domains. It has been shown that PTIP affects gene expression by controlling the activity of the transcription factor Pax2 and histone H3 lysine 4 methyltransferase complexes. In addition to its role in transcriptional regulation, PTIP has been implicated in DNA damage response. To ask if the depletion of PTIP affects the expression level of genes encoding DNA damage response factors , we compared the whole transcripts between wild-type and PTIP deficient chicken DT40 B cell lines.
Publication Title
PTIP promotes DNA double-strand break repair through homologous recombination.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 24 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The development of T cells has been characterized as taking place over three stages: nave (Tn), central memory (Tcm), and effector memory (Tem) cells.
Publication Title
Polarization diversity of human CD4+ stem cell memory T cells.
Sample Metadata Fields
Sex, Age
View Samples- Mus musculus
- 6 Downloadable Samples
- Ion Torrent Proton
Description
Growing evidences are suggesting that extra-long genes in mammals are vulnerable for full-gene length transcription and dysregulation of long genes is a mechanism underlying human genetic disorders. Skeletal muscle expresses Dystrophin which is 2.26 Mbp in length; however, how long-distance transcription is achieved is totally unknown. We had discovered RNA-binding protein SFPQ preferentially binds to long pre-mRNAs and specifically regulates the cluster of neuronal genes > 100 kbp. Here we investigated the roles of SFPQ for long gene expression, target specificities, and also physiological functions in skeletal muscle. Loss of Sfpq selectively downregulated genes >100 kbp including Dystrophin and caused progressive muscle mass reduction and metabolic myopathy characterized by glycogen accumulation and decreased abundance of mitochondrial oxidative phosphorylation complexes. Functional clustering analysis identified metabolic pathway related genes as the targets of SFPQ. These findings indicate target gene specificities and tissue-specific physiological functions of SFPQ in skeletal muscle. Overall design: We analyzed polyA-tailed RNA profiles including transcribing RNAs in gastrocnemius skeletal muscle ( from 3 control and 3 Sfpq-/- P35 male mice) using Ion-proton.
Publication Title
Loss of RNA-Binding Protein Sfpq Causes Long-Gene Transcriptopathy in Skeletal Muscle and Severe Muscle Mass Reduction with Metabolic Myopathy.
Sample Metadata Fields
Sex, Specimen part, Cell line, Subject
View Samples- Mus musculus
- 2 Downloadable Samples
- Ion Torrent Proton
Description
Growing evidences are suggesting that extra-long genes in mammals are vulnerable for full-gene length transcription and dysregulation of long genes is a mechanism underlying human genetic disorders. Skeletal muscle expresses Dystrophin which is 2.26 Mbp in length; however, how long-distance transcription is achieved is totally unknown. We had discovered RNA-binding protein SFPQ preferentially binds to long pre-mRNAs and specifically regulates the cluster of neuronal genes > 100 kbp. Here we investigated the roles of SFPQ for long gene expression, target specificities, and also physiological functions in skeletal muscle. Loss of Sfpq selectively downregulated genes >100 kbp including Dystrophin and caused progressive muscle mass reduction and metabolic myopathy characterized by glycogen accumulation and decreased abundance of mitochondrial oxidative phosphorylation complexes. Functional clustering analysis identified metabolic pathway related genes as the targets of SFPQ. These findings indicate target gene specificities and tissue-specific physiological functions of SFPQ in skeletal muscle. Overall design: We analyzed rRNA-depleted RNA profiles including transcribing RNAs in primary myoblasts obtained from skeletal muscles of 1-month-old SfpqSM-KO (n=1) and control (n=1) mice under differentiated condition using Ion-proton.
Publication Title
Loss of RNA-Binding Protein Sfpq Causes Long-Gene Transcriptopathy in Skeletal Muscle and Severe Muscle Mass Reduction with Metabolic Myopathy.
Sample Metadata Fields
Subject
View Samples