Kraus K W, Hallberg E M, Hallberg R
Mol Cell Biol. 1986 Nov;6(11):3854-61. doi: 10.1128/mcb.6.11.3854-3861.1986.
For Tetrahymena thermophila cells to survive extended periods of time at 43 degrees C, they must continuously synthesize heat shock proteins. For its translational machinery to function at 43 degrees C, T. thermophila requires either prior nonlethal heat shock treatment or brief treatment with partially inhibiting doses of cycloheximide or emetine. We have identified and characterized a mutant strain of T. thermophila (MC-3) in which prior nonlethal heat shock does not prevent protein synthesis inactivation at 43 degrees C. In addition, treatment of MC-3 cells with either of the antibiotics that normally confer 43 degrees C thermoprotection on wild-type cells elicited no similar thermoprotective response in these cells. Despite these phenotypic characteristics, by other criteria MC-3 synthesized a normal, functional array of heat shock proteins at 40 degrees C, a nonlethal heat shock protein-inducing temperature. The mutation in MC-3 which prevents the thermostabilization of protein synthesis by nonlethal heat shock is, by genetic criteria, most likely the same one which prevents the induction of thermotolerance by drug treatments. We present evidence that this mutation may affect some ribosome-associated functions.
嗜热四膜虫细胞要在43摄氏度下长时间存活，就必须持续合成热休克蛋白。为了使其翻译机制在43摄氏度下发挥作用，嗜热四膜虫需要事先进行非致死性热休克处理，或者用部分抑制剂量的环己酰亚胺或吐根碱进行短暂处理。我们已经鉴定并表征了嗜热四膜虫的一个突变株（MC - 3），在该突变株中，事先的非致死性热休克并不能防止43摄氏度下蛋白质合成的失活。此外，用通常能赋予野生型细胞43摄氏度热保护作用的任何一种抗生素处理MC - 3细胞，在这些细胞中都不会引发类似的热保护反应。尽管有这些表型特征，但按照其他标准，MC - 3在40摄氏度（一个非致死性热休克蛋白诱导温度）下合成了正常、功能性的热休克蛋白阵列。根据遗传学标准，MC - 3中阻止非致死性热休克使蛋白质合成热稳定的突变，很可能与阻止药物处理诱导耐热性的突变是同一个。我们提供的证据表明，这个突变可能会影响一些与核糖体相关的功能。
