Abstract

The phase resetting of the circadian oscillatory system by pulses of increased temperature (zeitgebers) and the temperature compensation of its period length during longer exposures are major features of the system, but are not well understood in molecular terms. In Neurospora crassa, the effects of pulses of increased temperature on the circadian rhythm of conidiation were determined and possible inputs to the oscillatory system tested, including changes in cyclic 3',5'-adenosine monophosphate (cAMP), inositol 1,4,5-trisphosphate and H+ concentrations, as well as changes of phosphorylation, synthesis and degradation of proteins. Following the kinetics of these parameters during exposure to increased temperature showed transient changes. Experimental manipulation of cAMP, Ca2+ and H+ levels, and of the synthesis and, possibly, degradation of proteins, resulted in phase shifts of the oscillatory system. It is assumed that the temperature signal affects the oscillator(s) by multiple pathways and shifts the whole state of the oscillatory system. Second messenger levels, protein synthesis and protein degradation show adaptation to longer exposures to elevated temperature which may be involved in the temperature compensation of the period length. The temperature compensation is also proposed to involve a shift in the state of all or most oscillator variables.

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