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Glycobiology Advance Access originally published online on January 19, 2005
Glycobiology 2005 15(6):649-654; doi:10.1093/glycob/cwi043
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Glycobiology vol. 15 no. 6 © Oxford University Press 2005; all rights reserved.

Testis-specific sulfoglycolipid, seminolipid, is essential for germ cell function in spermatogenesis

Yanlong Zhang2,3, Yoshihiro Hayashi4, Xinyao Cheng3, Tae Watanabe3, Xiangchun Wang3, Naoyuki Taniguchi1,3 and Koichi Honke1,2,5

2 Department of Molecular Genetics, Kochi University Medical School, Kochi 783-8505, Japan; 3 Department of Biochemistry, Osaka University Medical School, Osaka 565-0871, Japan; 4 Department of Pathology, Kochi University Medical School, Kochi 783-8505, Japan; and 5 CREST, Japan Science and Technology Agency, Japan


1 To whom correspondence should be addressed; e-mail: proftani{at}biochem.med.osaka-u.ac.jp; khonke{at}med.kochi-u.ac.jp

Received on December 13, 2004; revised on January 14, 2005; accepted on January 15, 2005

More than 90% of the glycolipid in mammalian testis consists of a unique sulfated glyceroglycolipid, seminolipid. The sulfation of the molecule is catalyzed by a Golgi membrane-associated sulfotransferase, cerebroside sulfotransferase (CST). Disruption of the Cst gene in mice results in male infertility due to the arrest of spermatogenesis prior to the metaphase of the first meiosis. However, the issue of which side of the cell function—germ cells or Sertoli cells—is deteriorated in this mutant mouse remains unknown. Our findings show that the defect is in the germ cell side, as evidenced by a transplantation analysis, in which wild-type spermatogonia expressing the green fluorescent protein were injected into the seminiferous tubules of CST-null testis. The transplanted GFP-positive cells generated colonies and spermatogenesis proceeded over meiosis in the mutant testis. The findings also clearly show that the seminolipid is expressed on the plasma membranes of spermatogonia, spermatocytes, spermatids, and spermatozoa, as evidenced by the immunostaining of wild-type testes using an anti-sulfogalactolipid antibody, Sulph-1 in comparison with CST-null testes as a negative control, and that seminolipid appears as early as day 8 of age, when Type B spermatogonia emerge.

Key words: cereboroside sulfotransferase / germ cell transplantation / green flourescent protein / knockout mouse / testis


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