In most previous termstem cellnext term systems, the organization of the previous termstem cell nichenext term and the anchoring matrix required for previous termstem cellnext term maintenance are largely unknown. We report here that collagen XVII (COL17A1/BP180/BPAG2), previous termanext term hemidesmosomal transmembrane collagen, is highly expressed in previous termhair follicle stem cellsnext term (HFSCs) and is required for the maintenance not only of HFSCs but also of previous termmelanocyte stem cellsnext term (MSCs), which do not express Col17a1 but directly adhere to HFSCs. Mice lacking Col17a1 show premature previous termhairnext term graying and previous termhairnext term loss. Analysis of Col17a1-null mice revealed that COL17A1 is critical for the self-renewal of HFSCs through maintaining their quiescence and immaturity, potentially explaining the mechanism underlying previous termhairnext term loss in human COL17A1 deficiency. Moreover, forced expression of COL17A1 in basal keratinocytes, including HFSCs, in Col17a1-null mice rescues MSCs from premature differentiation and restores TGF-β signaling, demonstrating that HFSCs function as previous termanext term critical regulatory component of the MSC previous termniche.next term