Premeiotic germ cell defect in seminiferous tubules of Atm-null testis

Keiyo Takubo, Atsushi Hirao, Masako Ohmura, Masaki Azuma, Fumio Arai, Go Nagamatsu, Toshio Suda

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Lifelong spermatogenesis is maintained by coordinated sequential processes including self-renewal of stem cells, proliferation of spermatogonial cells, meiotic division, and spermiogenesis. It has been shown that ataxia telangiectasia-mutated (ATM) is required for meiotic division of the seminiferous tubules. Here, we show that, in addition to its role in meiosis, ATM has a pivotal role in premeiotic germ cell maintenance. ATM is activated in premeiotic spermatogonial cells and the Atm-null testis shows progressive degeneration. In Atm-null testicular cells, differing from bone marrow cells of Atm-null mice, reactive oxygen species-mediated p16Ink4a activation does not occur in Atm-null premeiotic germ cells, which suggests the involvement of different signaling pathways from bone marrow defects. Although Atm-null bone marrow undergoes p16Ink4a-mediated cellular senescence program, Atm-null premeiotic germ cells exhibited cell cycle arrest and apoptotic elimination of premeiotic germ cells, which is different from p16Ink4a-mediated senescence.

Original languageEnglish
Pages (from-to)993-998
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume351
Issue number4
DOIs
Publication statusPublished - 2006 Dec 29

Keywords

  • ATM
  • Apoptosis
  • Cell cycle arrest
  • Premeiotic germ cells

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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  • Cite this

    Takubo, K., Hirao, A., Ohmura, M., Azuma, M., Arai, F., Nagamatsu, G., & Suda, T. (2006). Premeiotic germ cell defect in seminiferous tubules of Atm-null testis. Biochemical and Biophysical Research Communications, 351(4), 993-998. https://doi.org/10.1016/j.bbrc.2006.10.145