875 Ablation of Crif1 in hair follicle stem cells lead to hair growth retardation in adult mice

Abstract

Hair grows in a cyclical manner, in which anagen (growing phase), catagen (regression phase) and telogen (resting phase) are occurred periodically. The cyclicity of hair follicle indicates the presence of its own stem cells. Stem cells have a specific metabolic signature that is distinguished from the differentiated somatic cells. During the differentiation of hair follicle stem cells, mitochondria are elongated with more cristae and show higher activity, accompanying with activated aerobic respiration. Crif1 is a mitochondrial protein which regulates the synthesis and insertion of oxidative phosphorylation polypeptides by interacting with mitoribosomal large subunit. Recent studies reveal that conditional knockout of Crif1 in specific tissues of mice induced mitochondrial dysfunction. In this study, we investigated the effect of mitochondrial dysfunction in terms of Crif1 deficiency on the hair growth cycle and hair follicle stem cells in adult mice. Hair follicle specific inducible Crif1 conditional knockout (icKO) mice were generated by crossing K15-CrePR mice and Crif1 floxed mice (K15-CrePR;Crif1fl/fl). In Crif1 icKO mice, hair growth was significantly retarded compared to wild type littermates. However, hair follicle stem cell populations were not decreased significantly in Crif1 icKO mice. These results demonstrate that mitochondrial function in hair follicle stem cells is essential for the proceeding of hair growth cycle, but not for maintenance of hair follicle stem cells.