Disruption of Th2a and Th2b genes causes defects in spermatogenesis

Development
Toshie ShinagawaShunsuke Ishii

Abstract

The variant histones TH2A and TH2B are abundant in the testis, but their roles in spermatogenesis remain elusive. Here, we show that male mutant mice lacking both Th2a and Th2b genes were sterile, with few sperm in the epididymis. In the mutant testis, the lack of TH2B was compensated for by overexpression of H2B, whereas overexpression of H2A was not observed, indicating a decrease in the total histone level. Mutant mice exhibited two defects: incomplete release of cohesin at interkinesis after meiosis I and histone replacement during spermiogenesis. In the mutant testis, secondary spermatocytes at interkinesis accumulated and cohesin was not released normally, suggesting that the retained cohesion of sister chromatids delayed the subsequent entry into meiosis II. In addition, impaired chromatin incorporation of TNP2 and degenerated spermatids were observed in the mutant testis. These results suggest that a loss of TH2A and TH2B function in chromatin dynamics or a decrease in the total histone levels causes defects in both cohesin release and histone replacement during spermatogenesis.

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Citations

Dec 10, 2015·Stem Cells and Development·Linh My HuynhShunsuke Ishii
Jul 21, 2015·Biochemical and Biophysical Research Communications·Sivaraman PadavattanThirumananseri Kumarevel
Feb 7, 2016·Reproduction : the Official Journal of the Society for the Study of Fertility·Jianqiang Bao, Mark T Bedford
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Apr 8, 2017·Scientific Reports·Masashi HadaYuki Okada
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May 3, 2021·Clinical Epigenetics·Aniket PatankarPriyanka Parte
Nov 9, 2021·Frontiers in Endocrinology·Mélanie C FaurePascal Froment

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