Single-cell transcriptomic reconstruction of the human hair cycle: Capturing the temporal dynamics of skin tissue remodeling
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ABSTRACT:
PROVIDER: PRJNA995574 | ENA |
REPOSITORIES: ENA
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Project description:To investigate dynamic molecular and cellular changes associated with skin tissue remodeling during the human hair cycle, we aimed to obtain single-cell RNA sequencing (scRNA-seq) data from different hair cycle phases. We obtained scRNA-seq from randomly dissected human skin samples containing a single hair. Nineteen small skin pieces with a single hair were dissected from three female donors (single-hair samples). For comparison, we also collected three small skin pieces with no hairs from the same donors (non-hair samples). We enzymatically removed the interfollicular epidermis to focus our analysis on hair follicles and their surrounding dermis, which are the main areas of hair cycle-dependent tissue remodeling.
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Project description:Fgf18 gene is strongly expressed in hair follicles of mouse dorsal skin during regressing (catagen) and resting (telogen) phases of hair cycle, but not in growth (anagen) phase. This study aims at identifying the function of Fgf18 in the regulation of hair cycle. To define target genes of Fgf18 during telogen phase of hair cycle, we generated mice in which Fgf18 gene is conditionally knocked out in keratin 5-positive epithelial cells (referred to as Fgf18 cKO below). We carried out microarray experiments with mouse back skin samples harboring telogen hair follicles obtained from three 42-d-old Fgf18 cKO male mice, or from three 42-d-old C57BL/6 male mice as control. Total RNA was isolated from each mouse and further purified to polyA RNA using oligo dT30 columns. The RNA samples were pooled for each group. Gene expression was analyzed by one-color analysis using duplicate arrays for each group.
2017-05-15 | E-GEOD-29547 | biostudies-arrayexpress
Project description:Fgf18 gene is strongly expressed in hair follicles of mouse dorsal skin during regressing (catagen) and resting (telogen) phases of hair cycle, but not in growth (anagen) phase. This study aims at identifying the effects of FGF18 local delivery on the anagen phase of hair cycle. To define genes affected by local delivery of FGF18 during anagen phase of hair cycle, we injected FGF18 protein subcutaneously into back skin of C3H/HeN mice on day 4 of depilation-induced anagen. As control PBS was injected in place of FGF18. After 24 h (61-d-old), total RNA was isolated from the back skin and purified to poly A RNA. The RNA samples were pooled for each group. Gene expression was analyzed by one-color analysis using single array for each group.
2017-05-15 | E-GEOD-29546 | biostudies-arrayexpress
Project description:Fgf18 gene is strongly expressed in hair follicles of mouse dorsal skin during regressing (catagen) and resting (telogen) phases of hair cycle, but not in growth (anagen) phase. This study aims at identifying the function of Fgf18 in the regulation of hair cycle.
2017-05-15 | GSE29547 | GEO
Project description:Fgf18 gene is strongly expressed in hair follicles of mouse dorsal skin during regressing (catagen) and resting (telogen) phases of hair cycle, but not in growth (anagen) phase. This study aims at identifying the effects of FGF18 local delivery on the anagen phase of hair cycle.
2017-05-15 | GSE29546 | GEO
Project description:Telogen (resting phase) hair follicles are more radioresistant than anagen (growth phase) ones. Irradiation of BALB/c mice in the anagen phase with γ-rays at 6 Gy induced hair follicle dystrophy, whereas irradiation in the telogen phase induced the arrest of hair follicle elongation without any dystrophy after post-irradiation depilation. In contrast, FGF18 was highly expressed in the telogen hair follicles to maintain the telogen phase and also the quiescence of hair follicle stem cells. Therefore, the inhibition of FGF receptor signaling at telogen induced the dystrophy after post-irradiation depilation. In addition, the administration of recombinant FGF18 suppressed cell proliferation in the hair follicles and enhanced the repair of radiation-induced DNA damage, so FGF18 protected the anagen hair follicles against radiation damage to enhance hair regeneration. Moreover, FGF18 reduced the expression of cyclin B1 and cdc2 in the skin and FGF18 signaling induced G2/M arrest in the keratinocyte cell line HaCaT, although no obvious change of the expression of DNA repair genes was detected by DNA microarray analysis. These findings suggest that FGF18 signaling for the hair cycle resting phase causes radioresistance in telogen hair follicles by arresting the proliferation of hair follicle cells.
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Project description:Temporal Layering of Signaling Effectors Drives Chromatin Remodeling during Hair Follicle Stem Cell Lineage Progression
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Project description:Tissue regeneration relies on resident stem cells (SCs), whose activity and lineage choices are influenced by microenvironment. Exploiting the synchronized, cyclical bouts of tissue regeneration in hair follicles (HFs), we investigate how microenvironment dynamics shape the emergence of SC lineages. Employing epigenetic and ChIP-seq profiling, we uncover how signal-dependent transcription factors couple spatio-temporal cues to chromatin dynamics, thereby choreographing SC lineages. Using enhancer-driven reporters, mutagenesis and genetics, we show that simultaneous BMP-inhibitory and WNT signals set the stage for lineage choices by establishing chromatin platforms permissive for diversification. Mechanistically, when binding of BMP-effector pSMAD1 is relieved, super-enhancers driving HF-SC master regulators become silenced. Concomitantly, multipotent, lineage-fated super-enhancers silent in HF-SCs become activated by exchanging WNT-effectors TCF3/4 for LEF1. Throughout regeneration, lineage super-enhancers continue reliance upon LEF1, but then achieve specificity by accommodating additional incoming signaling effectors. Barriers to progenitor plasticity mount as diverse, signal-sensitive transcription factors shape LEF1-regulated super-enhancer dynamics.
2018-01-11 | GSE100875 | GEO
Project description:Tissue regeneration relies on resident stem cells (SCs), whose activity and lineage choices are influenced by microenvironment. Exploiting the synchronized, cyclical bouts of tissue regeneration in hair follicles (HFs), we investigate how microenvironment dynamics shape the emergence of SC lineages. Employing epigenetic and ChIP-seq profiling, we uncover how signal-dependent transcription factors couple spatio-temporal cues to chromatin dynamics, thereby choreographing SC lineages. Using enhancer-driven reporters, mutagenesis and genetics, we show that simultaneous BMP-inhibitory and WNT signals set the stage for lineage choices by establishing chromatin platforms permissive for diversification. Mechanistically, when binding of BMP-effector pSMAD1 is relieved, super-enhancers driving HF-SC master regulators become silenced. Concomitantly, multipotent, lineage-fated super-enhancers silent in HF-SCs become activated by exchanging WNT-effectors TCF3/4 for LEF1. Throughout regeneration, lineage super-enhancers continue reliance upon LEF1, but then achieve specificity by accommodating additional incoming signaling effectors. Barriers to progenitor plasticity mount as diverse, signal-sensitive transcription factors shape LEF1-regulated super-enhancer dynamics.
2018-01-11 | GSE100874 | GEO
Project description:Tissue regeneration relies on resident stem cells (SCs), whose activity and lineage choices are influenced by microenvironment. Exploiting the synchronized, cyclical bouts of tissue regeneration in hair follicles (HFs), we investigate how microenvironment dynamics shape the emergence of SC lineages. Employing epigenetic and ChIP-seq profiling, we uncover how signal-dependent transcription factors couple spatio-temporal cues to chromatin dynamics, thereby choreographing SC lineages. Using enhancer-driven reporters, mutagenesis and genetics, we show that simultaneous BMP-inhibitory and WNT signals set the stage for lineage choices by establishing chromatin platforms permissive for diversification. Mechanistically, when binding of BMP-effector pSMAD1 is relieved, super-enhancers driving HF-SC master regulators become silenced. Concomitantly, multipotent, lineage-fated super-enhancers silent in HF-SCs become activated by exchanging WNT-effectors TCF3/4 for LEF1. Throughout regeneration, lineage super-enhancers continue reliance upon LEF1, but then achieve specificity by accommodating additional incoming signaling effectors. Barriers to progenitor plasticity mount as diverse, signal-sensitive transcription factors shape LEF1-regulated super-enhancer dynamics.
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