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GSE1584
Mus musculus
3 Downloadable Samples
Affymetrix Mouse Expression 430A Array (moe430a)
Description
Mouse erythroid progenitors (EP) in comparison to granulocyte/monocyte - macrophage progenitors (GMP) from 10 - 16 week old C57/Bl6 - S129Ola (mixed genetic background) purified by flow cytometry
Publication Title
Prospective isolation and global gene expression analysis of the erythrocyte colony-forming unit (CFU-E).
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
MLL2, Not MLL1, Plays a Major Role in Sustaining MLL-Rearranged Acute Myeloid Leukemia.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 8 Downloadable Samples
Illumina HiSeq 2000
Description
APs were isolated from naïve skin and day 5wounds from dorsal skin wound beds of 7-9 weeks old using FACS. This experiment describes changes in AP gene expression associated with injury and subsequent tissue repair. Overall design: APs were isolated by FACS.
Publication Title
Myofibroblast proliferation and heterogeneity are supported by macrophages during skin repair.
Sample Metadata Fields
Sex, Age, Cell line, Subject
View Samples- Mus musculus
- 4 Downloadable Samples
- Illumina HiSeq 2000
Description
Cells were isolated from day 5wounds from dorsal skin wound beds of 7-9 weeks old using FACS. This experiment describes the gene expression profile associated with different immune cell subsets during tissue repair. Overall design: Cells were isolated by FACS.
Publication Title
Myofibroblast proliferation and heterogeneity are supported by macrophages during skin repair.
Sample Metadata Fields
Sex, Age, Cell line, Subject
View Samples- Mus musculus
- 16 Downloadable Samples
- Illumina HiSeq 2500, Illumina HiSeq 3000
Description
Host-environment interfaces such as the dermis comprise tissue macrophages as the most abundant resident immune cell type. Diverse tasks, i.e. to resist against invading pathogens, to attract bypassing immune cells from penetrating vessels and to aid tissue development and repair require a dynamic postnatal coordination of tissue macrophages specification. Here, we delineated the postnatal development of dermal macrophages and their differentiation into distinct subsets by adapting single cell transcriptomics, fate-mapping and tissue imaging. We thereby identified a small phenotypically and transcriptionally distinct subset of embryo-derived skin macrophages that was maintained and largely excluded from the overall postnatal exchange by monocytes. These macrophages specifically interacted with dermal sensory nerves, surveilled and trimmed the myelin sheets and regulated axon sprouting after mechanical injury. In summary, our data show long-lasting functional specification of macrophages in the dermis that is driven by step-wise adaptation to guiding structures and ensures codevelopment of ontogenetically distinct cells within the same compartment. Overall design: Single Cell Sequencing was performed on CD45+CD11b+CD64+Lin-(lineage B220, CD3, NK1.1, Siglec-F, Ly6G) CX3CR1 (low, mid, high) macrophage subsets from mouse dermis after enzymatic digestion
Publication Title
A Subset of Skin Macrophages Contributes to the Surveillance and Regeneration of Local Nerves.
Sample Metadata Fields
Age, Specimen part, Cell line, Subject
View Samples- Saccharomyces cerevisiae
- 47 Downloadable Samples
- Illumina HiSeq 2000
Description
Epigenetic mechanisms including histone post-translational modifications control longevity in diverse organisms. Relatedly, loss of proper transcriptional regulation on a global scale is an emerging aspect of shortened lifespan, but the specific mechanisms linking these observations remain to be uncovered. Here, we describe a lifespan screen in S. cerevisiae, designed to identify altered amino acid residues of histones that alter yeast replicative aging. Our results reveal that lack of sustained H3K36 methylation is commensurate with increased cryptic transcription in a set of genes in old cells and shorter lifespan. Deletion of the K36me2/3 demethylase Rph1 increases H3K36me3 within these genes and suppresses cryptic transcript initiation to extend lifespan. We show that this aging phenomenon is conserved, as cryptic transcription also increases in old worms. We propose that epigenetic misregulation in aging cells leads to an increase in transcriptional noise that is detrimental to lifespan, and, importantly, this acceleration in aging can be reversed by restoring transcriptional fidelity. Overall design: This study examines transcription in yeast aging using a WT or Rph1 mutant background over a sequence of time-dependent FACS sorts of old cells. Cryptic transcripts are detected using a small fragment sequencing approach. The youngest WT yeast (designated S1Y, S2Y) are represented in seven biological replicates and one technical replicate, five small fragment and three others; the oldest WT yeast (designated S4O) are also represented in seven biological replicates and one technical replicate, again composed of five small fragment samples and three others. Intermediate WT yeast aging sorts (S2O and S3O) are each represented by five biological replicates and one technical replicate, three small fragment and three others. For mutant yeast, each stage in the time series is represented by five biological replicates and one technical replicate, three small fragment and three others. Experiment 4 is a technical replicate of experiment 3.
Publication Title
H3K36 methylation promotes longevity by enhancing transcriptional fidelity.
Sample Metadata Fields
Subject
View Samples- Caenorhabditis elegans
- 4 Downloadable Samples
- NextSeq 500
Description
Epigenetic mechanisms including histone post-translational modifications control longevity in diverse organisms. Relatedly, loss of proper transcriptional regulation on a global scale is an emerging aspect of shortened lifespan, but the specific mechanisms linking these observations remain to be uncovered. Here, we describe a lifespan screen in S. cerevisiae, designed to identify altered amino acid residues of histones that alter yeast replicative aging. Our results reveal that lack of sustained H3K36 methylation is commensurate with increased cryptic transcription in a set of genes in old cells and shorter lifespan. Deletion of the K36me2/3 demethylase Rph1 increases H3K36me3 within these genes and suppresses cryptic transcript initiation to extend lifespan. We show that this aging phenomenon is conserved, as cryptic transcription also increases in old worms. We propose that epigenetic misregulation in aging cells leads to an increase in transcriptional noise that is detrimental to lifespan, and, importantly, this acceleration in aging can be reversed by restoring transcriptional fidelity. Overall design: This study examines transcription in worm aging using FUDR treatment. The samples represent a time-series, with one control group without FUDR, and then three treated with FUDR at days 1, 8, and 12. Days 8 and 12 represent old worms. There are no replicates.
Publication Title
H3K36 methylation promotes longevity by enhancing transcriptional fidelity.
Sample Metadata Fields
Cell line, Treatment, Subject
View Samples- Mus musculus
- 29 Downloadable Samples
- Illumina HiSeq 1500
Description
We here show that the niche regulates the quality of the hematopoietic stem cells (HSCs) that are regenerated after transplantation. We find that a reduced level of Wnt5a in the niche regenerates dysfunctional HSCs, which do not successfully engraft secondary recipients. In particular, RNA sequencing shows a dysregulated Zeb1-associated gene expression of multiple genes involved in the small GTPase-dependent actin polymerization pathway. Misexpression of these genes results in reduced ability to direct polarized F-actin localization, leading to defects in adhesion, migratory behavior and homing to the bone marrow of secondary recipients. Our study further shows that the Wnt5a-haploinsufficient environment similarly affects BCR-ABLp185+ cells, which, in 42% of the studied recipients, fail to generate leukemia and, in the remaining cases, fail to transfer leukemia to secondary hosts. Thus, we show that Wnt5a in the niche is required to regenerate HSCs and leukemic cells with functional ability to rearrange the actin cytoskeleton which is required for successful engraftment. Overall design: Hematopoietic stem cells are regenerated in WT or Wnt5a-haploinsufficient niches. We profile LSK hematopoiteic stem cells after transplantation and three cell populations from the niche environment: endothelial cells (EC), osteoblastic cells (OBC), and mesenchymal cells (MSC)
Publication Title
Niche WNT5A regulates the actin cytoskeleton during regeneration of hematopoietic stem cells.
Sample Metadata Fields
Cell line, Subject
View Samples- Danio rerio
- 12 Downloadable Samples
- Affymetrix Zebrafish Genome Array (zebrafish)
Description
Pbx homeodomain proteins have been implicated in the regulation of gene expression during muscle development. Whether Pbx proteins are required broadly for the regulation of muscle gene expression or are required for the expression of a specific subset of muscle gene expression is not known. We employed microarrays to determine the requirements for Pbx proteins during zebrafish development.
Publication Title
Pbx homeodomain proteins direct Myod activity to promote fast-muscle differentiation.
Sample Metadata Fields
No sample metadata fields
View Samples