Abstract
Sulfogalactosylglycerolipid (SGG) is the major sulfoglycolipid of male germ cells. During spermatogenesis, apoptosis occurs in >50% of total germ cells. Sertoli cells phagocytose these apoptotic germ cells and degrade their components using lysosomal enzymes. Here we demonstrated that SGG was a physiological substrate of Sertoli lysosomal arylsulfatase A (ARSA). SGG accumulated in Sertoli cells of Arsa(-/-) mice, and at 8 months of age, this buildup led to lysosomal swelling and other cellular abnormalities typical of a lysosomal storage disorder. This disorder likely compromised Sertoli cell functions, manifesting as impaired spermatogenesis and production of sperm with near-zero fertilizing ability in vitro. Fecundity of Arsa(-/-) males was thus reduced when they were older than 5 months. Sperm SGG is known for its roles in fertilization. Therefore, the minimal sperm fertilizing ability of 8-month-old Arsa(-/-) males may be explained by the 50% reduction of their sperm SGG levels, a result that was also observed in testicular germ cells. These unexpected decreases in SGG levels might be partly due to depletion of the backbone lipid palmitylpalmitoylglycerol that is generated from the SGG degradation pathway in Sertoli cells and normally recycled to new generations of primary spermatocytes for SGG synthesis.
Highlights
Sulfogalactosylglycerolipid (SGG) is the major sulfoglycolipid of male germ cells
SGG is synthesized in primary spermatocytes through sequential steps, including galactosylation of alkylacylglycerol by ceramide galactosyltransferase (CGT) to form galactosylglycerolipid (GG), which is sulfated by cerebroside sulfotransferase (CST) to form SGG [9, 10]
The ability of epididymal and vas deferens sperm from 8-month-old ArsaϪ/Ϫ males to bind to the zona pellucida (ZP) and to fertilize eggs in vitro was minimal compared with sperm from age-matched wild-type males (Fig. 1B)
Summary
Sulfogalactosylglycerolipid (SGG) is the major sulfoglycolipid of male germ cells. During spermatogenesis, apoptosis occurs in >50% of total germ cells. SGG accumulated in Sertoli cells of Arsa؊/؊ mice, and at 8 months of age, this buildup led to lysosomal swelling and other cellular abnormalities typical of a lysosomal storage disorder. The minimal sperm fertilizing ability of 8-month-old Arsa؊/؊ males may be explained by the 50% reduction of their sperm SGG levels, a result that was observed in testicular germ cells. These unexpected decreases in SGG levels might be partly due to depletion of the backbone lipid palmitylpalmitoylglycerol that is generated from the SGG degradation pathway in Sertoli cells and normally recycled to new generations of primary spermatocytes for SGG synthesis.—Xu, H., K. Mice genetically null for Cgt or Cst are infertile due to an arrest of spermatogenesis during pachytene spermatocyte development [11, 12]
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