Abstract: During spermatogenesis, the protein acetylation level regulated by both acetyltransferases (HATs) and histone deacetylases (HDACs) ensures the reconstruction of highly condensed chromatin and sperm motility. The acetyltransferase CREB-binding protein (CBP) and p300 can acetylate all the histones of H2A, H2B, H3 and H4, which can be blocked by the complex of inhibitor of acetyltransferases (INHAT). Testis-specific bromodomain (BRDT) protein, a conserved nucleoprotein member of the bromodomain and extra-terminal (BET) family, can recognize those acetylated or unacetylated histones. BRDT participates in the regulation of gene transcription in the early stage of spermatogenesis; BRDT can recognize the high-acetylated histones, which mediates the replacement from histone to protamine in the elongated spermatids. The deacetylated α-Tubulin, one of nonhistone proteins, impairs the sperm motility. Acetylation α-tubulin (Ac-α-Tu) is reduced in patients with asthenozoosperm.

Key words: Spermatogenesis, Histones, Epigenesis, genetic, Acetylation, Tubulin, Infertility, male