Gamma-ray irradiation promotes premature meiosis of spontaneously differentiating testis-ova in the testis of p53-deficient medaka (Oryzias latipes)

Cell Death Dis. 2012 Oct 4;3(10):e395. doi: 10.1038/cddis.2012.133.


In this study, the roles of p53 in impaired spermatogenic male germ cells of p53-deficient medaka were investigated by analyzing histological changes, and gene expressions of 42Sp50, Oct 4 and vitellogenin (VTG2) by RT-PCR or in situ hybridization in the testes. We found that a small number of oocyte-like cells (testis-ova) differentiated spontaneously in the cysts of type A and early type B spermatogonia in the p53-deficient testes, in contrast to the wild-type (wt) testes in which testis-ova were never found. Furthermore, ionizing radiation (IR) irradiation increased the number of testis-ova in p53-deficient testes, increased testis-ova size and proceeded up to the zygotene or pachytene stages of premature meiosis within 14 days after irradiation. However, 28 days after irradiation, almost all the testis-ova were eliminated presumably by p53-independent apoptosis, and spermatogenesis was restored completely. In the wt testis, IR never induced testis-ova differentiation. This is the first study to demonstrate the pivotal role of the p53 gene in the elimination of spontaneous testis-ova in testes, and that p53 is not indispensable for the restoration of spermatogenesis in the impaired testes in which cell cycle regulation is disturbed by IR irradiation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Differentiation / radiation effects
  • Gamma Rays*
  • Male
  • Meiosis / radiation effects*
  • Octamer Transcription Factor-3 / metabolism
  • Oryzias / growth & development
  • Peptide Elongation Factors / metabolism
  • Spermatogenesis / radiation effects
  • Spermatogonia / cytology*
  • Spermatogonia / metabolism
  • Spermatogonia / radiation effects
  • Testis / cytology
  • Testis / metabolism
  • Testis / pathology
  • Tumor Suppressor Protein p53 / deficiency
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism*
  • Vitellogenins / metabolism
  • Xenopus Proteins / metabolism


  • Octamer Transcription Factor-3
  • Peptide Elongation Factors
  • Tumor Suppressor Protein p53
  • Vitellogenins
  • Xenopus Proteins
  • thesaurin A