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GSE46368
Mus musculus
2 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Mouse lymphoma cells were co-cultured with endothelial cells in serum/cytokine-free condition. To identify specific genetic changes, we compared lymphoma cells cultured in medium containing 10% fetal bovine serum with lymphoma cells co-cultured with endothelial cells.
Publication Title
Angiocrine factors deployed by tumor vascular niche induce B cell lymphoma invasiveness and chemoresistance.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus, Homo sapiens
- 57 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Endothelial cells from nine steady state tissues and two regenerating tissues (bone marrow and liver) were intravitally labeld, isolated via flow sorting, and immediately processed for RNA extraction.
Publication Title
Molecular signatures of tissue-specific microvascular endothelial cell heterogeneity in organ maintenance and regeneration.
Sample Metadata Fields
Sex, Specimen part, Treatment, Time
View Samples- Mus musculus
- 17 Downloadable Samples
Illumina HiSeq 1000
Description
Mammalian spermatogonial stem cells (SSCs) spontaneously convert to multipotent adult spermatogonial-derived stem cells (MASCs) during in vitro expansion. Here, we examine the epigenetic signature of SSCs and MASCs, identifying bivalent histone H3-lysine4 and -lysine27 trimethylation at somatic gene promoters in SSCs and an ESC-like promoter chromatin state in MASCs. Overall design: Examination of gene expression in different cell types.
Publication Title
Epigenetic profiles signify cell fate plasticity in unipotent spermatogonial stem and progenitor cells.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 4 Downloadable Samples
- IlluminaHiSeq2000
Description
Analysis of gene expression of Pdx-EGFP1+ pancreatic progenitors before or after co-culture at mRNA level. The hypothesis tested in the study was that the overall gene expression in Pdx1-EGFP+ does not alter after co-culture with endothelial cells. The result supported our hypothesis. Overall design: Total RNA isolated from Pdx1-EGFP+ progenitors from the Pdx1-EGFP HUES8 cell-derived pancreatic progenitor population before (none) and after co-culture (AKT-HUVEC, MPEC, or BJ) Fig 2d in publication.
Publication Title
Endothelial cells control pancreatic cell fate at defined stages through EGFL7 signaling.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 4 Downloadable Samples
- Illumina HiSeq 2000, Illumina HiSeq 2500
Description
Bptf, a component of NURF chromatin-remodeling complex, is essential for maintaining the pool size and function of hematopoietic stem cells (HSCs). Genome-wide transcriptome profiling revealed that Bptf loss caused down-regulation of HSC-specific gene-expression programs, which included master transcription factors (such as Meis1, Pbx1, and Lmo2) known to be required for HSC maintenance and self-renewal. Bptf directly bound to the promoter of 'stemness' TF genes, potentiating their transcription and DNA accessibility. Overall design: To dissect the gene-regulatory role of Bptf in HSPCs, we sorted out phenotypically identical LSK cells from the bone marrow of Bptf conditional KO mice and littermate controls, followed by ACAT-seq and RNA-seq studies. We also performed H3K4me3 ChIP-seq using HPC7 cells, a murine HSPC-mimicking cell line.
Publication Title
The Chromatin Remodeler BPTF Activates a Stemness Gene-Expression Program Essential for the Maintenance of Adult Hematopoietic Stem Cells.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina HiSeq 2000
Description
Herein, we demonstrated that the cell lineage commitment is unexpectedly regulated by the novel functions of H2A.X, a histone variant which was only well-known for its role in genome integrity maintenance previously. Surprisingly, only in ESCs but not differentiated cells, H2A.X is specifically targeted to genomic regions encoding early embryonic and extra-embryonic lineage genes to repress their expression. In addition, H2A.X is also enriched at genomic regions sensitive to replication stress and maintains genomic stability thereat. Most interestingly, faithful H2A.X deposition plays critical roles in maintaining both cell lineage commitment and genome integrity in iPSC. In iPSC lines which support the development of "all-iPS" animals, H2A.X deposition faithfully recapitulates the ESC pattern and therefore, the genome stability and cell lineage commitment are maintained. In iPSC lines that fail to support embryonic development, defective H2A.X depositions result in aberrant upregulation of early embryonic and extra-embryonic lineage genes and H2A.X-dependent genome instability. Overall design: mRNA-Seq of WT ESC and H2A.X KO ESC; and 4N+, 4N- iPSC.
Publication Title
Histone variant H2A.X deposition pattern serves as a functional epigenetic mark for distinguishing the developmental potentials of iPSCs.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 24 Downloadable Samples
- Illumina HiSeq 2500
Description
Transplanting vascular endothelial cells (ECs) to support metabolism and express regenerative paracrine factors is a strategy to treat vasculopathies and to promote tissue regeneration. However, transplantation strategies have been challenging to develop because ECs are difficult to culture and little is known about how to sustain their vascular identity and direct them to form long-lasting new vessels or engraft into existing ones. We found that multiple non-vascular cell types transiently expressed EC markers after enforced expression of the transcription factors, Etv2, Erg, and Fli1. However, only mid-gestational amniotic cells could be converted to cells that maintained EC gene expression and proliferated in culture to yield billions of vascular cells. Even so, these converted cells performed sub-optimally in assays of EC function. We used constitutive Akt signaling to mimic the shear forces of the vascular environment and promote EC survival in an effort to correct the deficiencies of the converted cells. Akt signaling increased gene expression of EC morphogenesis genes, including Sox17, shifted the genomic targeting of Fli1 to favor nearby Sox consensus sites, and enhanced the in vivo vascular function of EC-like converted cells. Enforced expression of Sox17 was dispensable for broad EC gene activation, but indispensable for vascular engraftment and reperfusion of ischemic tissue. Our results identify a transcription factor network comprised of Ets and Sox17 factors that specifies and sustains endothelial cell fate and function. This work shows that the commonly used criterion of transcriptional similarity for cell conversion can fail to predict in vivo vascular function. Our approach shows that stringent functional testing in vitro and in vivo is necessary to validate engineered endothelial cell grafts. Overall design: Transcriptome sequencing of endothelial cells and amniotic cells
Publication Title
Sox17 drives functional engraftment of endothelium converted from non-vascular cells.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 5 Downloadable Samples
- Illumina HiSeq 2500
Description
Mature oocyte cytoplasm can reprogram somatic cell nuclei to the pluripotent state through a series of sequential events including protein exchange between the donor nucleus and ooplasm, chromatin remodeling, and pluripotency gene reactivation. Maternal factors that are responsible for this reprogramming process remain largely unidentified. Here, we demonstrate that knockdown of histone variant H3.3 in mouse oocytes results in compromised reprogramming and down-regulation of key pluripotency genes; and this compromised reprogramming both for developmental potentials and transcription of pluripotency genes can be rescued by injecting exogenous H3.3 mRNA, but not H3.2 mRNA into oocytes in somatic cell nuclear transfer (SCNT) embryos. We show that maternal H3.3, and not H3.3 in the donor nucleus, is essential for successful reprogramming of somatic cell nucleus into the pluripotent state. Furthermore, H3.3 is involved in this reprogramming process by remodeling the donor nuclear chromatin through replacement of donor nucleus-derived H3 with de novo synthesized maternal H3.3 protein. Our study shows that H3.3 is a crucial maternal factor for oocyte reprogramming and provides a practical model to directly dissect the oocyte for its reprogramming capacity. Overall design: Transcriptome sequencing of 4-cell NT embryos, Luciferase 4-cell SCNT embryos, 4-cell NT embryos_H3.3KD, 4-cell NT embryos_H3.3KD+H3.3mRNA, H3.3 KD + H3.2 mRNA SCNT embryos
Publication Title
Histone variant H3.3 is an essential maternal factor for oocyte reprogramming.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 27 Downloadable Samples
- Illumina HiSeq 2000
Description
We sequenced mRNA from individual stormal cells (Macrophages, Monocytes, and Neutrophils) and tumor epithelial cells from KrasG12dD; p53-/- murine lung cancer model and WT control mouse to compare gene expressio profiles of lung cancer stroma and tumor cells to their counterparts of WT lugns. The tumor was generated by injecting HKP1 lung cancer cell line, which was driven by KrasG12D activation and loss of p53, via tail vein. The cells were sorted by their specific surface markers at day 20-25 after orthortopic lung cancer formation. Overall design: Examination of mRNA levels in individual stormal cells and tumor cells from tumor lungs compared to their counterparts from WT lungs
Publication Title
Transcriptome analysis of individual stromal cell populations identifies stroma-tumor crosstalk in mouse lung cancer model.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 3 Downloadable Samples
- Illumina HiSeq 2000
Description
Polycomb repressive complex 2 (PRC2) regulates gene expression during lineage specification through trimethylation of lysine 27 on histone H3 (H3K27me3). In Drosophila, polycomb binding sites are dynamic chromatin regions coupled to incorporation of the histone variant H3.3. Here we show in mouse embryonic stem cells (ESCs) that H3.3 is required for proper establishment of H3K27me3 at the promoters of developmentally regulated genes. These promoters show reduced dynamics as determined by deposition of de novo synthesized histones, associated with reduced PRC2 occupancy. H3.3-depleted ESCs show upregulation of extraembryonic trophectoderm, as well as misregulation of other developmental genes upon differentiation. Our data demonstrate the importance of H3.3 incorporation in ESCs and suggest that changes in chromatin dynamics in its absence lead to misregulation of gene expression during differentiation. Moreover, our findings lend support to the emerging notion that H3.3 has multiple functions in distinct genomic locations that are not always correlated with an “active” chromatin state. Overall design: RNA-seq analysis of three embryonic stem cell lines (control, H3.3 KD1, and H3.3 KD2)
Publication Title
Hira-dependent histone H3.3 deposition facilitates PRC2 recruitment at developmental loci in ES cells.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples