Kallen K J, Quinn P, Allan D
Department of Physiology, University College London Medical School, UK.
Biochim Biophys Acta. 1993 Feb 24;1166(2-3):305-8. doi: 10.1016/0005-2760(93)90111-l.
The monovalent cationophore monensin, which is known to interfere with vesicular transport through the Golgi apparatus, inhibits synthesis of sphingomyelin in BHK cells by up to 40%. The monensin-sensitive component of sphingomyelin synthesis appears to be the pool which normally reaches the cell surface since treatment of cells with exogenous sphingomyelinase causes an almost identical loss of sphingomyelin. Monensin causes increases in ceramide and glucosylceramide labelling which together are equivalent to the decrease in sphingomyelin labelling. Monensin also increases synthesis of cholesterol ester, probably due to the decreased delivery of sphingomyelin to the plasma membrane. However, monensin has no effect on resynthesis of plasma membrane sphingomyelin which has been degraded by extracellular sphingomyelinase. The results support the idea that synthesis of sphingomyelin destined for the plasma membrane does not occur in the cis- or medial-Golgi but depends on vesicular transport of ceramide to a second synthesis site which is distal to the medial-Golgi.
单价阳离子载体莫能菌素已知会干扰通过高尔基体的囊泡运输，它能抑制BHK细胞中鞘磷脂的合成，抑制率高达40%。鞘磷脂合成中对莫能菌素敏感的成分似乎是正常情况下到达细胞表面的那部分储备，因为用外源性鞘磷脂酶处理细胞会导致鞘磷脂几乎等量减少。莫能菌素会使神经酰胺和葡萄糖神经酰胺标记增加，二者增加的总量与鞘磷脂标记的减少量相当。莫能菌素还会增加胆固醇酯的合成，这可能是由于鞘磷脂向质膜的转运减少所致。然而，莫能菌素对已被细胞外鞘磷脂酶降解的质膜鞘磷脂的再合成没有影响。这些结果支持了这样一种观点，即 destined for the plasma membrane 的鞘磷脂的合成并非发生在顺式或中间高尔基体中，而是依赖于神经酰胺通过囊泡运输到一个位于中间高尔基体远端的第二个合成位点。 （原英文中“destined for the plasma membrane”部分表述不太准确，推测可能是“运往质膜的”之类意思，翻译时按此理解处理，整体译文可能存在一定局限性，供参考）
