Gender Difference in Hair Length Revealed by CRISPR-Based Production of Long-Haired Mice with Dysfunctional FGF5 Mutations

October 2022 in “ International Journal of Molecular Sciences ”

Ryo Takahashi, Gou Takahashi, Yuichi Kameyama, Masahiro Sato, Masato Ohtsuka, Kenta Wada

CRISPR FGF5 Fgf5 mutant mice anagen phase androgen receptor hair cycle regulation frameshift mutations CRISPR gene editing fibroblast growth factor 5 hair growth phase male hormone receptor

Studysummary This study found that Fgf5 mutant mice exhibited longer hair, particularly in males, likely due to a prolonged anagen phase in the hair cycle.

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The study used CRISPR-based genome editing to create Fgf5 mutant mice, revealing gender differences in hair length due to dysfunctional FGF5 mutations. Male Fgf5go-malc1 mice exhibited significantly longer hair than females, attributed to frameshift mutations in the Fgf5 gene that disrupted the FGF5 protein and prolonged the anagen phase of hair growth. The research suggested a potential interaction between FGF5 and androgen receptor signaling, influencing hair growth and sexual dimorphism. The findings provided insights into the molecular mechanisms of hair cycle regulation and highlighted the role of FGF5 in hair growth.

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This study generated FGF5-knockout Dorper sheep using the CRISPR/Cas9 system, resulting in significantly increased fine-wool and active hair-follicle density, and explored downstream signaling pathways for potential applications in androgen alopecia treatment.

CRISPR/Cas9-Mediated Disruption of Fibroblast Growth Factor 5 in Rabbits Results in a Systemic Long Hair Phenotype by Prolonging Anagen

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This study found that FGF5-/- rabbits exhibited a significant long hair phenotype by prolonging the anagen phase, suggesting FGF5 acts as a negative regulator of hair growth.

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This study found that DKK1 and WNT10b are paracrine factors that modulate hair follicle stem cell differentiation inhibition, contributing to androgenetic alopecia by affecting Wnt signaling in androgen-sensitive dermal papilla cells after dihydrotestosterone stimulation.

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