Lack of a sulfated glycolipid results in male infertility: functional analyses in the testis of deficient mice

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More than 90% of the glycolipid in mammalian testis consists of a unique sulfated glycolipid, seminolipid. Seminolipid is synthesized by sequential action of the two enzymes, ceramide galactosyltransferase (CGT) and GalCer sulfotransferase (CST). Disruption of the Cgt and/or Cst gene in mice results in male infertility due to the arrest of spermatogenesis prior to the metaphase of the first meiosis. To clarify the process of germ cell degeneration in the absence of seminolipid, testicular lipids and proteins were analyzed in the wild-type and deficient mice. Age and genotype related changes were observed in some phospholipids. Proteomic analysis by two-dimensional DIGE showed that some protein spots were increased in the testis of deficient mice. Because seminolipid is expressed on the cell surface of primary spermatocytes, it was suggested that the lack of seminolipid may affect the formation of functional domains and/or cell junctions, which can mediate normal spermatogenesis.