Sadeghi H, Klein C
E.A. Doisy Department of Biochemistry, St. Louis University Medical School, Missouri 63104.
Differentiation. 1988 Jul;38(2):99-103. doi: 10.1111/j.1432-0436.1988.tb00203.x.
The aggregation program of Dictyostelium discoideum is extremely sensitive to the effects of tunicamycin when the drug is added to cells during the first few hours of starvation. Inhibition of development is observed with concentrations as low as 0.5 micrograms/ml, which cause only a 25%-30% inhibition of general N-linked glycosylation. However, 0.5 micrograms/ml tunicamycin can result in the total inhibition of N-linked glycosylation of specific, developmentally regulated, proteins, as exemplified by the glycoprotein 117 antigen. If added after the first hours of starvation, tunicamycin cannot inhibit aggregation even when present at 10 micrograms/ml, which maximally inhibits N-linked glycosylation. cAMP pulses can override the inhibitory effects of tunicamycin on cell aggregation. The data support the hypothesis that there is an early developmental pathway that is dependent on the N-linked glycosylation of one, or a small set of developmentally regulated proteins and that this pathway may involve the biogenesis of the chemotactic signalling system. In addition, the data raise questions as to the role of N-linked oligosaccharides in cell cohesion.
当在饥饿的最初几个小时将衣霉素添加到细胞中时,盘基网柄菌的聚集程序对衣霉素的作用极为敏感。浓度低至0.5微克/毫升时就可观察到发育受到抑制,而此浓度仅导致一般N-连接糖基化受到25%-30%的抑制。然而,0.5微克/毫升的衣霉素可导致特定的、受发育调控的蛋白质的N-连接糖基化完全受到抑制,糖蛋白117抗原就是例证。如果在饥饿最初几小时后添加衣霉素,即使其浓度高达10微克/毫升(此浓度可最大程度抑制N-连接糖基化)也无法抑制聚集。环磷酸腺苷脉冲可克服衣霉素对细胞聚集的抑制作用。这些数据支持这样的假说:存在一条早期发育途径,该途径依赖于一种或一小部分受发育调控的蛋白质的N-连接糖基化,并且此途径可能涉及趋化信号系统的生物合成。此外,这些数据还引发了关于N-连接寡糖在细胞黏附中作用的疑问。