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The epidermis, which consists mainly of keratinocytes, acts as a physical barrier to infections by regulating keratinocyte proliferation and differentiation. Hair follicles undergo continuous cycling to produce new one. Therefore, optimum supply of energy from the mitochondria is essential for maintaining skin homeostasis and hair growth. CRIF1 is a mitochondrial protein that regulates mitoribosome-mediated synthesis and insertion of mitochondrial oxidative phosphorylation polypeptides into the mitochondrial membrane in mammals. Recent studies reveal that conditional knockout (cKO) of  Crif1  in specific tissues of mice induced mitochondrial dysfunction. To determine whether the mitochondrial function of keratinocytes affects skin homeostasis and hair morphogenesis, we generated epidermis-specific  Crif1  cKO mice. Deletion of  Crif1  in epidermis resulted in impaired mitochondrial function and  Crif1  cKO mice died within a week. Keratinocyte proliferation and differentiation were markedly inhibited in  Crif1  cKO mice. Furthermore, hair follicle morphogenesis of  Crif1 c KO mice was disrupted by down-regulation of Wnt/β-catenin signaling. These results demonstrate that mitochondrial function in keratinocytes is essential for maintaining epidermal homeostasis and hair follicle morphogenesis.

Targeted deletion of Crif1 in mouse epidermis impairs skin homeostasis and hair morphogenesis