Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA318648 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3394990.fastq.gz | Fastqsanger.gz | |||
| SRR3394991.fastq.gz | Fastqsanger.gz | |||
| SRR3394992.fastq.gz | Fastqsanger.gz | |||
| SRR3394993.fastq.gz | Fastqsanger.gz | |||
| SRR3394994.fastq.gz | Fastqsanger.gz |
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Project description:Cell proliferation is essential to rapid tissue growth and repair, but is inherently associated with considerable genome damage that cells must efficiently prevent or fix to prevent cell cycle arrest. Here, we implicate the transcription factor Gata6 in regulation of adult mouse hair follicle regeneration where it controls the renewal of the rapidly proliferating epithelial (matrix) progenitors and hence the extent of production of terminally differentiated lineages. We find that Gata6 protects against DNA damage associated with proliferation, thus preventing cell cycle arrest and apoptosis. Furthermore, we show that Gata6 stimulates the Eddarad/NF-kB pathway, important for DNA-damage repair and stress response in general, and for hair follicle growth in particular. Finally, we find Edaradd essential, downstream of Gata6 for cell survival and proliferation. Our data add to recent evidence in embryonic stem and neural progenitor cells, suggesting a model whereby developmentally regulated transcription factors protect from DNA damage associated with proliferation occurring at key stages of rapid tissue growth. Our data may aid in understanding why Gata6 is a frequent target of amplification in cancers.
2016-12-15 | GSE80354 | GEO
Project description:Posttranslational protein modifications have emerged as a mechanism regulating progenitor cell state transitions during tissue formation. Herein, we exploit the stereotyped hair follicle development to delineate the function of PADI4; an enzyme converting peptidylarginine to citrulline. Single cell-sequencing places Padi4 in both progenitor and differentiated hair lineage cells and indicate that PADI4 acts to repress transcription during hair follicle development. We establish PADI4 as a negative regulator of proliferation, acting on LEF1-positive hair shaft committed progenitor cells. Mechanistically, PADI4 citrullinates proteins associated with mRNA-processing and ribosomal biogenesis, and lack of PADI4 promotes protein synthesis and rRNA transcription in vivo. Characterizing key translational effectors, we demonstrate that PADI4 citrullinates the translational repressor 4E-BP1 and reveal a crosstalk between PADI4 activity and 4E-BP1 phosphorylation. This work sheds new light on how posttranslational modifications impact progenitor cell states and tissue formation.
2025-07-28 | PXD064137 | Pride
Project description:MTD project_description Inflammation and decreased stem cell function characterize organism aging, yet the relationship between these factors remains incompletely understood. This study shows that aged hematopoietic stem and progenitor cells exhibit increased ground-stage NF-κB activity, which enhances their responsiveness to undergo differentiation and loss of self-renewal in response to inflammation. The study identifies Rad21/cohesin as a critical mediator of NF-κB signals, by increasing chromatin accessibility of inter-/intra-genic and enhancer regions. Rad21/NF-κB are required for normal differentiation, but limit self-renewal of hematopoietic stem cells (HSCs) during aging and inflammation in an NF-κB dependent manner. HSCs from aged mice fail to downregulate Rad21/cohesin and inflammation/differentiation inducing signals in the resolution phase after acute inflammation. and The inhibition of cohesin/NF-κB is sufficient to revert the hypersensitivity of aged HSPCs to inflammation-induced differentiation. During aging, myeloid-biased HSCs with disrupted and naturally occurring reduced expression of Rad21/cohesin are increasingly selected over lymphoid-biased HSCs. Together, Rad21/cohesin mediated NF-κB signaling limits HSPC function during aging and selects for cohesin deficient HSCs with myeloid skewed differentiation.
2018-11-28 | PXD011537 | Pride
Project description:Mouse hair follicles undergo synchronized cycles. Cyclical regeneration and hair growth is fueled by stem cells (SCs). During the rest phase, the HF-SCs remain quiescent due to extrinsic inhibitory signals within the niche. As activating cues accumulate, HF-SCs become activated, proliferate, and grows downward to form transient-amplifying matrix progenitor cells. We used ChIP-seq to reveal the genome-wide maps of histone modifications underlying the states of hair follicle stem cells and their transient-amplifying progeny before differentiation. Quiescent hair follicle stem cells (qHF-SCs), activated hair follicle stem cells (aHF-SCs) and transient-amplifying matrix cells (HF-TACs) were FACS-purified for ChIP-sequcencing.
2011-09-02 | E-GEOD-31239 | biostudies-arrayexpress
Project description:Mouse hair follicles (HFs) undergo synchronized cycles. Cyclical regeneration and hair growth is fueled by stem cells (SCs). During the rest phase, the HF-SCs remain quiescent due to extrinsic inhibitory signals within the niche. As activating cues accumulate, HF-SCs become activated, proliferate, and grow downward to form transient-amplifying matrix progenitor cells. We used microarrays to detect the relative levels of global gene expression underlying the states of hair follicle stem cells and their transient-amplifying progeny before differentiation. Quiescent hair follicle stem cells (qHF-SCs), activated hair follicle stem cells (aHF-SCs) and transient-amplifying matrix cells (HF-TACs) were FACS-purified for RNA extraction and hybridization on Affymetrix microarrays. To obtain homogeneous populations of expression profiles, we applied the FACS technique to purify SC and TACs according to their cell surface markers.
2011-09-01 | E-GEOD-31028 | biostudies-arrayexpress
Project description:Tissue formation requires a coordinated balance of progenitor cell proliferation and differentiation. Posttranslational protein modifications have emerged as a mechanism utilized to regulate progenitor cell state transitions. Herein, we exploit the well characterized and stereotyped hair follicle development to delineate the function of PADI4; an enzyme converting peptidylarginine to citrulline. Single cell-sequencing places Padi4 in both progenitor and differentiated hair lineage cells during hair follicle development. We show that the absence of PADI4 induces gene expression across hair follicle cell clusters, suggesting that PADI4 acts to negatively impact transcription. In addition, we establish PADI4 as a negative regulator of proliferation, acting of LEF1-positive hair shaft committed progenitor cells. Mechanistically, PADI4 citrullinates proteins associated with mRNA-processing and ribosomal biogenesis, and lack of PADI4 promotes protein synthesis and rRNA transcription in vivo, in both hair follicle progenitor and committed lineage cells. Characterizing key translational effectors, we demonstrate that PADI4 interacts with 4E-BP1 and reveal a crosstalk between PADI4 activity and 4E-BP1 phosphorylation. We report that PADI4 contributes to hair follicle development by repressing progenitor cell proliferation and translational activity. This work sheds new light on how posttranslational modifications impact progenitor cell states and tissue formation.
2025-07-28 | GSE288124 | GEO
Project description:Quiescent hair follicle (HF) bulge stem cells (SCs) differentiate to early progenitor (EP) hair germ (HG) cells, which divide to produce transit-amplifying (TA) matrix cells. EPs can revert to SCs upon injury, but whether this de-differentiation occurs in normal HF homeostasis (hair cycle), and the mechanisms regulating both differentiation and de-differentiation are unclear. Here we use lineage tracing, gain of function, transcriptional profiling, and functional assays to examine the role of observed endogenous Runx1 level changes in the hair cycle. We find that forced Runx1 expression implements hair degeneration (catagen) and simultaneously promotes changes in the quiescent bulge SC transcriptome towards a cell-state resembling the EP HG fate. This cell-state transition is functionally reversible. We propose that SC differentiation and de-differentiation are likely to occur during normal HF degeneration and niche restructuring in response to changes in endogenous Runx1 levels associated with SC location with respect to the niche. Freshly isolated skin cells were FACS sorted based on K15-GFP+/a6-integrin+/CD34- as hair germ and K15-GFP+/a6-integrin+/CD34+ bulge cells. Duplicate samlpes from mice at PD20 that showed telogen morphology throughout skin were used for RNA prepartion and Affymetrix analysis. Wild and transgenic samples after 1-day of doxycycline treatement were compared.
2014-01-15 | E-GEOD-53077 | biostudies-arrayexpress
Project description:Mouse back skin was disassociated to single cells, sorted by cell surface markers and tested by microarrray To compare the gene expression of mouse bulge (CD34+CD200+CD49+) versus secondary hair germ (CD34-CD200+CD49+) versus interfollicular epidermis (CD34-CD200-CD49+) xx Bald scalp retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells Androgenetic alopecia (AGA) or common baldness results from a marked decrease in hair follicle size. This miniaturization may be related to loss of hair follicle stem or progenitor cells. To test this hypothesis, we analyzed bald and non-bald scalp from the same individuals for the presence of hair follicle stem and progenitor cells using flow cytometry to quantitate cells expressing CYTOKERATIN 15 (KRT15), CD200, CD34 and ALPHA-6-INTEGRIN (ITGA6). High levels of KRT15 expression correlated with stem cell properties of small cell size and quiescence. Cells with the highest level of KRT15 expression were maintained in bald scalp; however, distinct populations of CD200high ITGA6high cells and CD34-positive cells were markedly diminished. Consistent with a progenitor cell phenotype, the diminished populations localized closely to the stem-cell rich bulge area but were larger and more proliferative than the bulge stem cells. In functional assays, analogous CD200 high /Itga6 high cells from murine hair follicles were multipotent and generated new hair follicles in skin reconstitution assays. These findings suggest that a defect in stem cell activation plays a role in the pathogenesis of AGA. 4 independent biologic replicates (each pooled from 3 distinct mice) were sorted for Mouse bulge (CD34+CD200+CD49+) versus secondary hair germ (CD34-CD200+CD49+) versus interfollicular epidermis (CD34-CD200-CD49+)
2011-01-12 | E-GEOD-21568 | biostudies-arrayexpress
Project description:In this setup gene profiling of hair follicle keratinocytes with active nuclear NF-κB is used to further analyze the role of NF-κB in HF development. For this purpose an NF-κB-responsive EGFP reporter mouse has been constructed, which enables in vivo visualization of cells with NF-κB activity and their isolation via fluorescence assisted cell sorting (FACS). The isolated cells were used to establish a gene profile of early hair placode keratinocytes with NF-κB activity (E14.5).
2016-02-29 | E-MTAB-4535 | biostudies-arrayexpress
Project description:Mouse hair follicles undergo synchronized cycles. Cyclical regeneration and hair growth is fueled by stem cells (SCs). During the rest phase, the HF-SCs remain quiescent due to extrinsic inhibitory signals within the niche. As activating cues accumulate, HF-SCs become activated, proliferate, and grows downward to form transient-amplifying matrix progenitor cells. We used ChIP-seq to reveal the genome-wide maps of histone modifications underlying the states of hair follicle stem cells and their transient-amplifying progeny before differentiation.
2011-09-02 | GSE31239 | GEO