title: Abnormal sperm morphology caused by defects in Sertoli cells of Cnot7 knockout mice.
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.
authors.affiliation: Department of Urology, Yokohama City University Graduate School of Medicine, Yokohama, Japan. ogawa@med.yokohama-cu.ac.jp
authors.forename: Takehiko
authors.initials: T
authors.lastname: Ogawa
authors.forename: Chizuru
authors.initials: C
authors.lastname: Ito
authors.forename: Takahisa
authors.initials: T
authors.lastname: Nakamura
authors.forename: Yoichi
authors.initials: Y
authors.lastname: Tamura
authors.forename: Tadashi
authors.initials: T
authors.lastname: Yamamoto
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Noda
authors.forename: Yoshinobu
authors.initials: Y
authors.lastname: Kubota
authors.forename: Kiyotaka
authors.initials: K
authors.lastname: Toshimori
mesh_terms: D000818:Animals; D017690:Cell Transplantation; D005095:Exoribonucleases; D017353:Gene Deletion; D005854:Germ Cells / Q000648:ultrastructure; D049452:Green Fluorescent Proteins / Q000378:metabolism; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D009845:Oligospermia / Q000209:etiology; D011506:Proteins / Q000235:genetics*; D012097:Repressor Proteins; D012260:Ribonucleases; D012671:Seminiferous Tubules / Q000378:metabolism / Q000648:ultrastructure; D012708:Sertoli Cells / Q000473:pathology* / Q000648:ultrastructure; D013087:Spermatids / Q000473:pathology / Q000648:ultrastructure; D013091:Spermatogenesis; D013094:Spermatozoa / Q000002:abnormalities*; D013737:Testis / Q000648:ultrastructure
chemical_list: D011506:Proteins; D012097:Repressor Proteins; D049452:Green Fluorescent Proteins; C489778:Cnot7 protein, mouse; D005095:Exoribonucleases; D012260:Ribonucleases