Nishikawa Y
Tokyo Metropolitan Institute of Medical Science, Japan.
Biochim Biophys Acta. 1991 Jan 31;1091(2):135-40. doi: 10.1016/0167-4889(91)90052-y.
I have previously isolated a temperature-sensitive FM3A mutant (G258) defective in asparagine-linked glycosylation. G258 shows not only the temperature sensitivity for cell growth, but also temperature sensitivity for synthesis of oligosaccharide-lipid (Nishikawa, Y. (1984) J. Cell. Physiol. 119, 260-266). In the present study, I isolated revertants for cell growth from G258 cells. All three growth revertants also showed reversion on the synthesis of oligosaccharide-lipid. These results imply that the temperature sensitivity for oligosaccharide-lipid synthesis of G258 couples with the temperature sensitivity for cell growth of the mutant. A possible mechanism of the coupling between impaired oligosaccharide-lipid synthesis and growth arrest of G258 cells at 39 degrees C is discussed.
我之前分离出了一种对温度敏感的FM3A突变体(G258),其天冬酰胺连接的糖基化存在缺陷。G258不仅对细胞生长表现出温度敏感性,对寡糖脂的合成也表现出温度敏感性(西川洋,(1984年)《细胞生理学杂志》119卷,260 - 266页)。在本研究中,我从G258细胞中分离出了细胞生长回复突变体。所有三个生长回复突变体在寡糖脂合成方面也表现出回复。这些结果表明,G258对寡糖脂合成的温度敏感性与该突变体对细胞生长的温度敏感性相关联。本文讨论了在39摄氏度时,G258细胞中受损的寡糖脂合成与生长停滞之间可能的关联机制。