TY - JOUR
T1 - Effects of constant light on circadian rhythmicity in mice lacking functional cry genes
T2 - Dissimilar from per mutants
AU - Spoelstra, Kamiel
AU - Daan, Serge
N1 - Funding Information:
Acknowledgments Our work is supported by the EC’s 5th frame-work project BRAINTIME (QLRT-2001-01829) and the 6th Frame-work Project EUCLOCK (No. 018741). We are grateful to Dr. Urs Albrecht and Dr. Bert van der Horst for the original stocks of mPer mutants and mCry mutants, respectively. We thank Gerard J. F. Overkamp for expert technical support, and several reviewers for constructive comments.
PY - 2008
Y1 - 2008
N2 - Mutations in each of the genes mPer1, mPer2, mCry1 and mCry2 separately cause deviations from the wild type circadian system. Differences between these mutant strains have inspired the hypothesis that the duality of circadian genes (two mPer and two mCry genes involved) is related to the existence of two components in the circadian oscillator (Daan et al., J Biol Rhythms 16:105-116, 2001). We tested the predictions from this theory that the circadian period (τ) lengthens under constant illumination (LL) in mCry1 and mPer1 mutant mice, while it shortens in mCry2 and mPer2 mutants. mCry1 -/- and mCry2 -/- knockout mice both consistently increased τ with increasing light intensity, as did wild type mice. With increasing illumination, rhythmicity is reduced in mCry1, mCry2 and mPer1, but not in mPer2 deficient mice. Results for mPer mutant mice are in agreement with data reported on these strains earlier by Steinlechner et al. (J Biol Rhythms 17:202-209, 2002), and also with the predictions from the model. The increase in cycle length of the circadian system by light in the mCry2 deficient mice violates the predictions. The model is thereby rejected: the mCry genes do not play a differential role, although the opposite responses of mPer mutants to light remain consistent with a functional Evening-Morning differentiation.
AB - Mutations in each of the genes mPer1, mPer2, mCry1 and mCry2 separately cause deviations from the wild type circadian system. Differences between these mutant strains have inspired the hypothesis that the duality of circadian genes (two mPer and two mCry genes involved) is related to the existence of two components in the circadian oscillator (Daan et al., J Biol Rhythms 16:105-116, 2001). We tested the predictions from this theory that the circadian period (τ) lengthens under constant illumination (LL) in mCry1 and mPer1 mutant mice, while it shortens in mCry2 and mPer2 mutants. mCry1 -/- and mCry2 -/- knockout mice both consistently increased τ with increasing light intensity, as did wild type mice. With increasing illumination, rhythmicity is reduced in mCry1, mCry2 and mPer1, but not in mPer2 deficient mice. Results for mPer mutant mice are in agreement with data reported on these strains earlier by Steinlechner et al. (J Biol Rhythms 17:202-209, 2002), and also with the predictions from the model. The increase in cycle length of the circadian system by light in the mCry2 deficient mice violates the predictions. The model is thereby rejected: the mCry genes do not play a differential role, although the opposite responses of mPer mutants to light remain consistent with a functional Evening-Morning differentiation.
KW - Constant light
KW - Cry1
KW - Cry2
KW - Per1
KW - Per2
U2 - 10.1007/s00359-007-0301-3
DO - 10.1007/s00359-007-0301-3
M3 - Article
C2 - 18057941
AN - SCOPUS:41749084887
SN - 0340-7594
VL - 194
SP - 235
EP - 242
JO - Journal of Comparative Physiology A: Neuroethology, Sensory, Neural, and Behavioral Physiology
JF - Journal of Comparative Physiology A: Neuroethology, Sensory, Neural, and Behavioral Physiology
IS - 3
ER -