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哺乳动物培养成纤维细胞中昼夜节律的温度补偿和温度重置

Temperature compensation and temperature resetting of circadian rhythms in mammalian cultured fibroblasts.

作者信息

Tsuchiya Yoshiki, Akashi Makoto, Nishida Eisuke

机构信息

Department of Cell and Developmental Biology, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto 606-8502, Japan.

出版信息

Genes Cells. 2003 Aug;8(8):713-20. doi: 10.1046/j.1365-2443.2003.00669.x.

Abstract

BACKGROUND

Circadian rhythms control many physiological processes. One of characteristic properties of circadian rhythms is insensitivity to temperature, called temperature compensation. Although this temperature-insensitive property has repeatedly been observed mainly in circadian output rhythms, temperature effect on autoregulatory feedback loops of clock gene expression, the rhythm-generating mechanisms, has not been fully investigated.

RESULTS

We show first that the circadian oscillation of clock gene expression in NIH3T3 fibroblasts, which is induced by TPA (12-O-tetradecanoylphorbol-13-acetate) treatment, is strongly temperature-compensated over the temperature range of 33-42 degrees C. We then show that heat treatment at 42 degrees C is able to trigger circadian oscillation of clock gene expression in NIH3T3 cells. This 42 degrees C heat treatment, unlike serum shock or TPA treatment, did not induce immediate expression of mPer1 mRNA, suggesting the existence of several different resetting mechanisms.

CONCLUSIONS

This is the first demonstration of temperature compensation of the rhythm-generating core feedback loops of clock gene expression in mammalian cultured cells. It is possible that cells in the periphery could sense the change of ambient temperature as a resetting cue and that the whole organism thus could be entrained rapidly at dawn, in cooperation with the resetting mechanism by light.

摘要

背景

昼夜节律控制着许多生理过程。昼夜节律的一个特征特性是对温度不敏感,称为温度补偿。尽管这种温度不敏感特性主要在昼夜输出节律中反复被观察到,但温度对时钟基因表达的自动调节反馈回路(节律产生机制)的影响尚未得到充分研究。

结果

我们首先表明,由佛波酯(12 - O - 十四酰佛波醇 - 13 - 乙酸酯)处理诱导的NIH3T3成纤维细胞中时钟基因表达的昼夜振荡在33 - 42摄氏度的温度范围内具有很强的温度补偿性。然后我们表明,42摄氏度的热处理能够触发NIH3T3细胞中时钟基因表达的昼夜振荡。这种42摄氏度的热处理与血清休克或佛波酯处理不同,不会诱导mPer1 mRNA的立即表达,这表明存在几种不同的重置机制。

结论

这是首次在哺乳动物培养细胞中证明时钟基因表达的节律产生核心反馈回路的温度补偿。外周细胞有可能将环境温度的变化感知为一种重置线索,从而整个生物体可以在黎明时与光的重置机制协同快速被同步。

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