Abnormal sperm morphology caused by defects in Sertoli cells of Cnot7 knockout mice

Takehiko Ogawa, Chizuru Ito, Takahisa Nakamura, Yoichi Tamura, Tadashi Yamamoto, Tetsuo Noda, Yoshinobu Kubota, Kiyotaka Toshimori

Research output: Contribution to journalArticlepeer-review

14 Citations (Scopus)

Abstract

Cnot7 is a co-factor of transcription regulation, expressed in a variety of tissues including the lung, liver, thyroid gland, and testis. Our previous study (Nakamura et al., 2004) showed that deletion of the Cnot7 gene in mice caused almost no abnormal phenotypes except for male infertility, due to oligo-astheno-teratozoospermia. This study also showed that Cnot7-/- mouse germ cells transplanted as donors could colonize in recipient wild mouse testes to develop normal spermatogenesis by spermatogonial transplantation assay, suggesting that the abnormal spermatogenesis observed in the Cnot7-/- testes was induced by the impaired testicular microenvironment rather than a germ cell defect. In the present study, we have carried out reciprocal germ cell transplantation in which wild type germ cells were transplanted as donors into the recipient Cnot7-/- testes to evaluate the recipient microenvironment for supporting the spermatogenesis of donor cells. We noticed that donor cell colonization was less efficient in Cnot7-/- than in Cnot7-/-testes, and that the donor derived spermatids in the recipient Cnot7-/- testes showed severe deformities. These results support our previous report that Sertoli cell defects in the Cnot7-/- testes could induce oligo-astheno-teratozoospermia.

Original languageEnglish
Pages (from-to)307-314
Number of pages8
Journalarchives of histology and cytology
Volume67
Issue number4
DOIs
Publication statusPublished - 2004 Nov
Externally publishedYes

ASJC Scopus subject areas

  • Histology

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