Yoshiki Tsuchiya1, Makoto Akashi, Eisuke Nishida. 1. Department of Cell and Developmental Biology, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto 606-8502, Japan.
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.
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.
Authors: Charna Dibner; Daniel Sage; Michael Unser; Christoph Bauer; Thomas d'Eysmond; Felix Naef; Ueli Schibler Journal: EMBO J Date: 2008-12-11 Impact factor: 11.598