North M J
J Bacteriol. 1974 Nov;120(2):741-7. doi: 10.1128/jb.120.2.741-747.1974.
The glycerol kinase activity induced by incubation of Neurospora crassa at low temperatures was rapidly lost when cultures were returned to 26 C. After a short lag, the activity disappeared irreversibly with a half-life of approximately 15 min. The loss of activity was not due to a change in the level of an inhibitor or activator. Glycerol reduced the activity loss but did not completely prevent it, which was an effect that was dependent on protein synthesis. The cold-induced activity was also always lost on addition of cycloheximide at all temperatures tested (0 to 26 C), which indicated continuous inactivation, although cycloheximide did not affect the actual rate of activity loss at 26 C. The basal glycerol kinase activity was not sensitive to cycloheximide. The mechanism responsible for inactivation was destroyed by sonic oscillation. The process is not thought to play a role in the cold-induced increase in activity. Glycerol kinase activity induced at 26 C by glycerol was also lost on addition of cycloheximide and after addition of sucrose.
将粗糙脉孢菌在低温下培养诱导产生的甘油激酶活性,当培养物回到26℃时会迅速丧失。经过短暂的延迟后,该活性以约15分钟的半衰期不可逆地消失。活性丧失并非由于抑制剂或激活剂水平的变化。甘油可减少活性丧失,但不能完全阻止,这一效应依赖于蛋白质合成。在所有测试温度(0至26℃)下添加环己酰亚胺时,冷诱导的活性也总是丧失,这表明存在持续失活,尽管环己酰亚胺不影响26℃时活性丧失的实际速率。基础甘油激酶活性对环己酰亚胺不敏感。导致失活的机制会被声波振荡破坏。该过程被认为在冷诱导的活性增加中不起作用。在26℃由甘油诱导产生的甘油激酶活性在添加环己酰亚胺后以及添加蔗糖后也会丧失。