Kurosawa Gen, Iwasa Yoh
Department of Biology, Faculty of Sciences, Kyushu University, Fukuoka-shi, Fukuoka 812-8581, Japan.
J Theor Biol. 2005 Apr 21;233(4):453-68. doi: 10.1016/j.jtbi.2004.10.012. Epub 2004 Dec 25.
Circadian clock of organisms has a free-running period that does not change much with ambient temperature. This property "temperature compensation" is studied when the rate of all reaction steps increase with temperature in the biochemical network generating the rhythm. The period becomes shorter when all the rate parameters are enhanced by the same factor. However, the period becomes longer as degradation rate of proteins and/or transcription rate of the clock gene increase (their elasticity is positive). This holds for a wide range of models, including N-variable model, and PER-TIM double oscillator model, provided that (1) branch reactions (e.g. degradation of proteins or mRNAs) are strongly saturated, and that (2) the cooperativity of transcription inhibition by nuclear proteins is not very large. A strong temperature sensitivity of degradation of PER proteins and/or temperature-sensitive alternative splicing of per gene, known for Drosophila, can be mechanisms for the temperature compensation of circadian clock.
生物体的昼夜节律时钟具有一个自由运行周期，该周期不会随环境温度发生太大变化。当在产生节律的生化网络中所有反应步骤的速率随温度增加时，就会对这种“温度补偿”特性进行研究。当所有速率参数都以相同因子增强时，周期会变短。然而，随着蛋白质的降解速率和/或时钟基因的转录速率增加（它们的弹性为正），周期会变长。这适用于广泛的模型，包括N变量模型和PER-TIM双振荡器模型，前提是：（1）分支反应（例如蛋白质或mRNA的降解）强烈饱和，以及（2）核蛋白对转录抑制的协同性不是很大。果蝇中已知的PER蛋白降解的强温度敏感性和/或per基因的温度敏感可变剪接，可能是昼夜节律时钟温度补偿的机制。
