Abstract
Hair follicle stem cells (HFSCs) are multipotent cells that cycle through quiescence and activation to continuously fuel the production of hair follicles. Prior genome mapping studies had shown that tri-methylation of histone H3 at lysine 27 (H3K27me3), the chromatin mark mediated by Polycomb Repressive Complex 2 (PRC2), is dynamic between quiescent and activated HFSCs, suggesting that transcriptional changes associated with H3K27me3 might be critical for proper HFSC function. However, functional in vivo studies elucidating the role of PRC2 in adult HFSCs are lacking. In this study, by using in vivo loss-of-function studies we show that, surprisingly, PRC2 plays a non-instructive role in adult HFSCs and loss of PRC2 in HFSCs does not lead to loss of HFSC quiescence or changes in cell identity. Interestingly, RNA-seq and immunofluorescence analyses of PRC2-null quiescent HFSCs revealed upregulation of genes associated with activated state of HFSCs. Altogether, our findings show that transcriptional program under PRC2 regulation is dispensable for maintaining HFSC quiescence and hair regeneration.
Highlights
Hair follicles (HFs) undergo cycles of growth, destruction, and rest throughout an organism’s lifetime [1]
Hair follicle stem cells (HFSCs) have the incredible capacity to cycle through quiescence and activation to fuel the production of hair follicles throughout the life of an organism
This balance between HFSC activation and quiescence is maintained by establishing a specific transcriptional landscape; very little is known about how chromatin-modifying factors, critical regulators of gene transcription, control adult HFSC function
Summary
Hair follicles (HFs) undergo cycles of growth (anagen), destruction (catagen), and rest (telogen) throughout an organism’s lifetime [1]. This cyclical regeneration is fueled by hair follicle stem cells (HFSCs) that reside in the niche called the bulge, where they remain in a quiescent state influenced by the incoming extrinsic inhibitory signals [1,2]. During telogen-to-anagen transition, the dermal papilla (DP), located below the bulge, provides activating cues that signal the HFSCs to briefly proliferate and produce differentiating transit amplifying cells (HF-TAC) that give rise to a new HF before returning to the quiescent state [3]. Very little is known about how chromatin modifying factors, critical regulator of gene transcription, control HFSC function and hair regeneration in the adult skin. PRC2 complex facilitates the tri-methylation of histone H3 at lysine 27 (H3K27me3) modification, which results in gene repression [8,9]
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