Inhibition of testicular germ cell apoptosis and differentiation in mice misexpressing Bcl-2 in spermatogonia

Takemitsu Furuchi, Kazue Masuko, Yoshitake Nishimune, Masuo Obinata, Yasuhisa Matsui

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127 Citations (Scopus)


During normal spermatogenesis, more than half of the germ cells undergo apoptosis, but the physiological significance and molecular mechanisms of this programmed cell death are largely unknown. Because Bcl-2 functions as a death repressor, we have investigated the effect of misexpressing Bcl-2 in spermatogonia in transgenic mice using the human bcl-2 cDNA under the control of the human polypeptide chain elongation factor 1α (EF-1α) promoter. In the 2-week-old transgenic testes, exogenous Bcl-2 was expressed in spermatogonia and massive accumulation of spermatogonia was observed in seminiferous tubules by 4 weeks. At this time, only a few spermatocytes were apparent, and the accumulated cells degenerated, leading to vacuolization in some seminiferous tubules by 7 weeks. In older transgenic mice, abnormal accumulation of spermatogonia and degeneration of these germ cells was still observed, but some seminiferous tubules in which the level of Bcl-2 expression was reduced recovered normal spermatogenesis. These observations indicate that spermatogonial apoptosis is part of the normal program of mammalian spermatogenesis and is regulated by a pathway affected by Bcl-2.

Original languageEnglish
Pages (from-to)1703-1709
Number of pages7
Issue number6
Publication statusPublished - 1996 Jul 5


  • Apoptosis
  • Bcl-2
  • Spermatogenesis
  • Spermatogonia
  • Transgenic mice

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology


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