Haak D, Gable K, Beeler T, Dunn T
Department of Biochemistry, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA.
J Biol Chem. 1997 Nov 21;272(47):29704-10. doi: 10.1074/jbc.272.47.29704.
The Saccharomyces cerevisiae SCS7 and SUR2 genes are members of a gene family that encodes enzymes that desaturate or hydroxylate lipids. Sur2p is required for the hydroxylation of C-4 of the sphingoid moiety of ceramide, and Scs7p is required for the hydroxylation of the very long chain fatty acid. Neither SCS7 nor SUR2 are essential for growth, and lack of the Scs7p- or Sur2p-dependent hydroxylation does not prevent the synthesis of mannosyldiinositolphosphorylceramide, the mature sphingolipid found in yeast. Deletion of either gene suppresses the Ca2+-sensitive phenotype of csg2Delta mutants, which arises from overaccumulation of inositolphosphorylceramide due to a defect in sphingolipid mannosylation. Characterization of scs7 and sur2 mutants is expected to provide insight into the function of ceramide hydroxylation.
酿酒酵母的SCS7和SUR2基因是一个基因家族的成员，该家族编码使脂质去饱和或羟基化的酶。Sur2p是神经酰胺鞘氨醇部分C-4羟基化所必需的，而Scs7p是超长链脂肪酸羟基化所必需的。SCS7和SUR2对生长都不是必需的，并且缺乏Scs7p或Sur2p依赖的羟基化并不妨碍甘露糖基二肌醇磷酸神经酰胺的合成，甘露糖基二肌醇磷酸神经酰胺是酵母中发现的成熟鞘脂。删除任何一个基因都能抑制csg2Delta突变体的Ca2+敏感表型，该表型是由于鞘脂甘露糖基化缺陷导致肌醇磷酸神经酰胺过度积累而产生的。对scs7和sur2突变体的表征有望为神经酰胺羟基化的功能提供深入了解。
