Abstract

Temperature compensation is an important property of all biological clocks. In Neurospora crassa, negative-feedback regulation on the frequency (frq) gene's transcription by the FRQ protein plays a central role in the organism's circadian pacemaker. Earlier model calculations predicted that the stability of FRQ should determine the period length of Neurospora's circadian rhythm as well as the rhythm's temperature compensation. Here, we report experimental FRQ protein stabilities in frq mutants at 20 degrees C and 25 degrees C, and estimates of overall activation energies for mutant FRQ protein degradation. The results are consistent with earlier model predictions, i.e., temperature compensation of Neurospora's circadian rhythm is a highly regulated process where the stability of FRQ is an important factor in determining Neurospora's circadian period as well as the clock's temperature compensation. The partial loss of temperature compensation in frq7 and frq(S513I) mutants can be described by a simple negative-feedback model (the Goodwin oscillator) when the experimentally obtained activation energies of FRQ degradation for theses mutants are incorporated into the model.