title: Temperature compensation and temperature resetting of circadian rhythms in mammalian cultured fibroblasts.
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.
authors.affiliation: Department of Cell and Developmental Biology, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto 606-8502, Japan.
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Tsuchiya
authors.forename: Makoto
authors.initials: M
authors.lastname: Akashi
authors.forename: Eisuke
authors.initials: E
authors.lastname: Nishida
mesh_terms: D000818:Animals; D056926:CLOCK Proteins; D002273:Carcinogens / Q000494:pharmacology; D018797:Cell Cycle Proteins; D002940:Circadian Rhythm / Q000187:drug effects / Q000502:physiology*; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism*; D005786:Gene Expression Regulation; D051379:Mice; D041681:NIH 3T3 Cells; D009687:Nuclear Proteins / Q000378:metabolism; D056950:Period Circadian Proteins; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013696:Temperature; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D013997:Time Factors; D015534:Trans-Activators / Q000235:genetics / Q000378:metabolism*; D014157:Transcription Factors; D014158:Transcription, Genetic
chemical_list: D002273:Carcinogens; D018797:Cell Cycle Proteins; D009687:Nuclear Proteins; C539023:Per1 protein, mouse; C513312:Per2 protein, mouse; C512645:Per3 protein, mouse; D056950:Period Circadian Proteins; D012333:RNA, Messenger; D015534:Trans-Activators; D014157:Transcription Factors; D056926:CLOCK Proteins; C538944:Clock protein, mouse; D013755:Tetradecanoylphorbol Acetate