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

哺乳动物睾丸中90%以上的糖脂是由一种独特的硫酸化糖脂--异麦芽糖脂组成。精脂是通过神经酰胺半乳糖基转移酶（CGT）和半乳糖苷磺基转移酶（CST）这两种酶的顺序作用合成的。小鼠中Cgt和/或Cst基因的破坏由于在第一次减数分裂中期之前精子发生的停滞而导致雄性不育。为了阐明在不存在胆固醇脂质的情况下生殖细胞变性的过程，在野生型和缺陷型小鼠中分析了睾丸脂质和蛋白质。在一些磷脂中观察到年龄和基因型相关的变化。二维DIGE蛋白质组学分析表明，缺陷小鼠睾丸中的一些蛋白质点增加。由于精母细胞表面表达精脂，因此认为精脂的缺乏可能会影响功能域和/或细胞连接的形成，这些功能域和/或细胞连接可以介导正常的精子发生。

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.