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Significance Androgen plays essential roles for sex differentiation of external genitalia through regulating male-biased genes. Even females can differentiate into male-type external genitalia depending on the degree of androgenic exposure. However, the mechanisms underlying androgen responsiveness in females are poorly defined. Here, we demonstrate Sp1 regulates the enrichment of H3K27ac on androgen receptor-mediated regulatory elements in both males and females, indicating transcriptional competency for male-biased genes is conserved by Sp1 in both sexes. Compound- MafB mutant mice lacking a tissue-specific enhancer in the MafB 3′ UTR show incomplete male-type external differentiation similar to female-type differentiation. These findings underscore the idea that transcriptional competency for male-biased genes is preserved in both sexes, thus helping define the potential sexual fate of external genitalia.
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Kajioka et al. (2021) studied this question.
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