Transcriptome analysis of hair follcile stem cell quiescence
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA552097 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9624590_1.fastq.gz | Fastqsanger.gz | |||
| SRR9624590_2.fastq.gz | Fastqsanger.gz | |||
| SRR9624583_1.fastq.gz | Fastqsanger.gz | |||
| SRR9624583_2.fastq.gz | Fastqsanger.gz | |||
| SRR9624584_1.fastq.gz | Fastqsanger.gz |
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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
Project description:Open chromatin analysis of hair follcile stem cell quiescence
| PRJNA552095 | ENA
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
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
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.
2016-02-05 | GSE67404 | GEO
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.
2013-10-28 | GSE51765 | GEO
Project description:Chronic, sustained exposure to stressors can profoundly impact tissue homeostasis, although the mechanisms by which these changes occur are largely unknown. Here, we report the adrenal gland-derived stress hormone corticosterone (the rodent equivalent of cortisol) regulates hair follicle stem cell (HFSC) quiescence and hair growth in mice. Without systemic corticosterone, HFSCs enter substantially more rounds of the regeneration cycle throughout life. Conversely, under chronic stress, elevated corticosterone levels prolong HFSC quiescence and keep hair follicles in an extended resting phase. Mechanistically, corticosterone acts on dermal papilla (DP) to suppress the expression of a secreted factor, Growth Arrest Specific 6 (Gas6). Restoring Gas6 expression overcomes stress-induced inhibition of HFSC activation and hair growth. Our work identifies corticosterone as a systemic inhibitor of HFSC activity via its impact on the niche, and demonstrates that removal of such inhibition drives HFSCs into frequent regeneration cycles with no observable defects long-term.
2021-02-13 | GSE135705 | GEO
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
2013-10-30 | GSE51635 | GEO
Project description:The transition of stem cells from a quiescent state to an active state is a finely tuned process that requires the dismantling of the quiescence program and the establishment of a cell cycle-promoting transcriptional landscape. Whether epigenetic processes control stem cell states to promote the regeneration of adult tissues remains elusive. In this study, we show that a repressive histone modification, H2AK119ub, is dynamic between quiescent and active hair follicle stem cells (HFSCs) in the adult murine skin. Ablation of H2AK119ub in HFSCs leads to failure in maintaining quiescence leading to premature activation and an eventual exhaustion of HFSC pool. Transcriptional and chromatin studies revealed that H2AK119ub directly represses a proliferation promoting transcriptional program in the HFSCs to preserve quiescence. Lastly, we identify that the inhibitory FGF signaling produced by the hair follicle niche keratinocytes maintains H2AK119ub in quiescent HFSCs. Together, these findings reveal that a repressive histone mark, H2AK119ub, is under the dynamic regulation of inhibitory niche signaling to prevent the untimely establishment of an activated state to preserve SC function and longevity.
2025-10-13 | GSE279014 | GEO
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