The relationship between FRQ-protein stability and temperature compensation in the Neurospora circadian clock

被引:111
|
作者
Ruoff, P [1 ]
Loros, JJ
Dunlap, JC
机构
[1] Univ Stavanger, Dept Math & Nat Sci, N-4036 Stavanger, Norway
[2] Dartmouth Coll Sch Med, Dept Biochem, Hanover, NH 03755 USA
[3] Dartmouth Coll Sch Med, Dept Genet, Hanover, NH 03755 USA
关键词
FREQUENCY protein;
D O I
10.1073/pnas.0505137102
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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 frq(7) and frq(S5131) 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.
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页码:17681 / 17686
页数:6
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