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Open chromatin analysis of hair follcile stem cell quiescence

ABSTRACT: Tissue stem cells are required for homeostasis and wound repair throughout the entire lifespan. Multiple mechanisms have been extensively studied for the maintenance of stem cell quiescence. Here we use Omini-ATACseq and single cell ATACseq to study the stem cell quiescence at epigenetic level. We sought out to compare the open chromatin state in different cell lineages between control and Foxc1/Nfatc1 double knockout mice. The single cell ATACseq could further help infer the transcription regulation between enhancers and promoters interaction.

ORGANISM(S): Mus musculus

PROVIDER: GSE133646 | GEO | 2021/09/30

REPOSITORIES: GEO

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Transcriptome analysis of hair follcile stem cell quiescence

Project description:Hair follicle stem cells(HFSCs) can transition between active and quiescent stages during normal hair cycle or would healing. Transcriptional regulation has been show to regulate the transition. Previous studies have shown that two transcription factor, Foxc1 and Nfatc1, can help maintain the stem cells in quiescent state, the deletion of either one could lead to precocious activation. Here, we collect the hair follicle stem cell at postnatal day 30 from both control mice, Nfatc1 knockout mice, Foxc1 knockout mice(downloaded) and Foxc1/Nfatc1 double knockout mice to study the transcriptional regulation network of HFSCs quiescence.

2021-09-30 | GSE133647 | GEO

Foxc1 reinforces quiescence in hair follicle stem cells

Project description:Quiescent stem cells are periodically activated to maintain tissue homeostasis or occasionally called into action upon injury. Molecular mechanisms that constitutively maintain stem cell identity or promote stem cell proliferation and differentiation upon activation have been extensively studied. However, it is unclear how quiescent stem cells maintain identity and reinforce quiescence when they transition from quiescence to activation. Here we show mouse hair follicle stem cell compartment induces a transcription factor, Foxc1, when activated. Importantly, deletion of Foxc1 in the activated but not quiescent stem cells compromises stem cell identity, fails to re-establish quiescence and subsequently drives premature stem cell activation.These findings uncover a dynamic, cell-intrinsic mechanism employed by hair follicle stem cells to reinforce stemness in response to activation. Poly(A)-enriched transcriptome RNA-seq on HFSCs isolated in WT and K14Cre cKO mice at anagen and early telogen stage of hair cycle.

2016-02-05 | E-GEOD-67404 | biostudies-arrayexpress

Foxc1 reinforces quiescence in hair follicle stem cells

2016-02-05 | GSE67404 | GEO

Open chromatin analysis of hair follcile stem cell quiescence

Project description:Open chromatin analysis of hair follcile stem cell quiescence

| PRJNA552095 | ENA

Global analysis of genome accessibility in hair follicle stem cells

2016-02-05 | GSE68288 | GEO

Single cell transcriptomic analysis of aging hair follicles

Project description:Tissue stem cells are required for homeostasis and wound repair throughout the entire lifespan. Multiple mechanisms have been extensively studied for the maintenance of stem cell. Here we use single cell RNAseq to study the stem cell maintenance during aging. We sought out to compare the gene expression changes in different cell lineages between control, Foxc1/Nfatc1 double knockout mice and aging mice.

2021-09-30 | GSE145654 | GEO

Transcriptome analysis of hair follcile stem cell quiescence

Project description:Transcriptome analysis of hair follcile stem cell quiescence

| PRJNA552097 | ENA

Stem cell quiescence acts as a tumor suppressor mechanism in hair follicle initiated squamous tumors

Project description:In many organs, adult stem cells are uniquely poised to serve as cancer cells of origin. In the epidermis, hair follicle stem cells (HFSCs) cycle through stages of quiescence (telogen) and proliferation (anagen) to drive hair growth. Within the hair follicle, HFSCs are capable of initiating squamous cell carcinoma, yet it is unclear how the hair cycle contributes to tumorigenesis. The data presented here show that HFSCs are unable to initiate tumors during the quiescent phase of the hair cycle, indicating that the mechanisms that keep HFSCs dormant are dominant to gain of oncogenes (Ras) or loss of tumor suppressors (p53). Instead, prolonged oncogenic stimuli only exert their effects when HFSC quiescence mechanisms are removed by normal HFSC activation. Furthermore, Pten activity is necessary for quiescence based tumor suppression, since Pten deletion alleviates this stem cell specific ability without affecting proliferation per se. Small RNAs were cloned from Trizol-lysed cells sorted from mouse skin and sequenced with the Illumina HiSeq2000.

2013-10-28 | E-GEOD-51765 | biostudies-arrayexpress

Stem Cell Quiescence acts as a tumor suppressor mechanism in hair follicle initiated squamous tumors

Project description:In some organs, adult stem cells are uniquely poised to serve as cancer cells of origin1-4. It is unclear, however, whether tumorigenesis is influenced by the activation state of the adult stem cell. Hair follicle stem cells (HFSCs) act as cancer cells of origin for cutaneous squamous cell carcinoma (SCC) and undergo defined cycles of quiescence and activation. The data presented here show that HFSCs are unable to initiate tumors during the quiescent phase of the hair cycle, indicating that the mechanisms that keep HFSCs dormant are dominant to the gain of oncogenes (Ras) or the loss of tumor suppressors (p53). Furthermore, Pten activity is necessary for quiescence based tumor suppression, as its deletion alleviates tumor suppression without affecting proliferation. These data demonstrate that stem cell quiescence is a form of tumor suppression in HFSCs, and that Pten plays a role in maintaining quiescence in the presence of tumorigenic stimuli. This experiment includes RNA profiling of hair follicle stem cells at various stages of tumorigenesis Briefly: HFSCs were lineage traced with YFP allele, FACS isolated from various genotypes, and then profiled by Affymetrix microarray Cell Isolation and FACS: Whole dorsal and ventral mouse K15-CrePR; LSLYFP, K15-CrePR; KrasG12D; LSLYFP and K15-CrePR; KrasG12D; Ptenff; LSLYFP was extracted, diced and digested with collagenase (20mg/ml) for 2 hours at 37C, then an equal volume of .25% trypsin was added and digestion continued for an additional hour at 37C. Digested tissue was mechanically dispersed via pipette and filtered with a 100uM cell strainer, collected at 300g and washed twice with PBS. The cells were then filtered through a 40uM cell strainer and FACS processed. YFP+ and YFP- cell populations were collected in RNA lysis buffer (Stratagene) and stored at -80C. Gene expression profiling Microarray analyses by GeneSpring software were performed

2013-10-30 | E-GEOD-51635 | biostudies-arrayexpress

Dietary restriction delays but cannot heal irradiation-induced hair graying by preserving hair follicle stem cells in quiescence

Project description:DNA damage represents one of the cell intrinsic causes of stem cell aging, which leads to differentiation induced removal of damaged stem cells in skin and blood. Dietary restriction (DR) retards aging across various species including several strains of laboratory mice. Whether, DR has the potential to ameliorate DNA damage driven stem cell exhaustion remains incompletely understood. Here, we show that DR strongly extends the time to hair graying in response to γ–irradiation (IR) induced DNA damage of C57BL/6J mice. The study shows that DR prolongs quiescence of hair follicle stem cells (HFSCs) by silencing gene regulatory networks and metabolic switches that control proliferation and tissue regeneration. DR-mediated prolongation of HSFC quiescence blocks hair growth and prevents the depletion of HFSCs and ckit+ melanoblasts in response to IR. However, prolongation of HSFCs quiescence also leads to a suppression of DNA repair pathways and cannot prevent melanoblast loss and hair graying in the long run, when hair cycling is re- initiated even after extended periods of time. Together, these results support a model indicating that nutrient deprivation can delay but not heal DNA damage driven extinction of HFSCs and melanoblasts by stalling HSFCs in a prolonged state of quiescence coupled with inhibition of DNA repair. Disconnecting these two types of responses to DR could have the potential to delay stem cell aging.

2024-02-21 | GSE156014 | GEO

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