Skin repair after injury involves the recruitment of undifferentiated progenitor cells from nearby hair follicles (HFs) into the regenerating epidermis. The bulge and the secondary hair germ of HFs contain distinct populations of epithelial stem cells, and now Vladimir Botchkarev and co-workers reveal that the Lim-homeodomain transcription factor Lhx2 differentially regulates these populations during wound healing (). They show that, in mice, most of the cells that proliferate in response to skin injury in the HF bulge and secondary hair germ express Lhx2. Wound re-epithelisation is retarded in Lhx2+/– mice compared with wild-type mice, they report, whereas the onset of active hair growth in HFs near to the wound is accelerated. Other experiments indicate that Lhx2 promotes wound re-epithelisation by upregulating Sox9 and Tcf4 expression in the bulge cells while simultaneously inhibiting HF cycling by downregulating Lgr5 expression in the secondary hair germ. Thus, Lhx2 is a key regulator of the differential response of HF stem cells during epidermal regeneration after injury.
