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Publication : Histological characterization of defective spermatogenesis in mice lacking the basigin gene.

First Author  Toyama Y Year  1999
Journal  Anat Histol Embryol Volume  28
Issue  3 Pages  205-13
PubMed ID  10458027 Mgi Jnum  J:103143
Mgi Id  MGI:3608554 Doi  10.1046/j.1439-0264.1999.00194.x
Citation  Toyama Y, et al. (1999) Histological characterization of defective spermatogenesis in mice lacking the basigin gene. Anat Histol Embryol 28(3):205-13
abstractText  Basigin is a transmembrane protein belonging to the immunoglobulin superfamily. In the light of the fact that knockout mice lacking the basigin gene (Bsg) are azoospermic, the phenotype in the male reproductive system was extensively examined in this study. Spermatogenesis in Bsg (-/-) mice was found to be disrupted, and arrested at the metaphase of the first meiotic division. A few germ cells differentiated into young spermatids, but they were exfoliated. The lumens of the male reproductive system were filled with round degenerated cells. Using the TUNEL method and electron microscopy, some of the degenerated cells in the testis and epididymal head were shown to be apoptotic. Crystalloids of fine tubules and unusual ectoplasmic specializations were also observed in the Sertoli cells of Bsg (-/-) mice. These specializations displayed unusual 'circular' structures. Furthermore, unusual ectoplasmic specializations covering the spermatocytes rather than the mature spermatids were found. These structures were formed as a result of the lack of mature spermatids in the Bsg (-/-) testis. Results from analyses of azoospermia in the Bsg (-/-) mice suggest that basigin, through the interactions between germ cells and Sertoli cells, is an essential factor in the growth and/or survival of spermatids.
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