GSE171662
Lgr6 marks epidermal stem cells with a nerve-dependent role in wound re- epithelialization
Stem cells support the lifelong maintenance of adult organs but their specific roles during injury are poorly understood. Here, we demonstrate that Lgr6 marks a regionally restricted population of epidermal stem cells that interact with nerves and specialize in wound re-epithelialization. Diphtheria toxin-mediated ablation of Lgr6 stem cells delays wound healing, and skin denervation phenocopies this effect. Using intravital imaging to capture stem cell dynamics after injury, we show that wound re-epithelialization by Lgr6 stem cells is diminished following the loss of nerves. This induces the recruitment of other stem cell populations, including hair follicle stem cells, which partially compensate to mediate the wound closure. Single-cell lineage tracing and gene expression analysis reveal that the fate of Lgr6 stem cells is shifted towards differentiation following the loss of their niche. We conclude that Lgr6 epidermal stem cells are primed for injury response and interact with nerves to regulate their fate Overall design: mRNA profiling of FACS-sorted untreated or denervated Lgr6-GFP+-Tomato+-Itga6+ mouse dorsal epidermal stem cells