NDLI: The mouse Clock mutation reduces circadian pacemaker amplitude and enhances efficacy of resetting stimuli and phase

Content Provider	PubMed Central
Author	Hotz, Vitaterna Martha Ko, Caroline H. Chang, Anne-marie Buhr, Ethan D. Fruechte, Ethan M. Schook, Andrew Antoch, Marina P. Turek, Fred W. Takahashi, Joseph S.
Copyright Year	2006
Abstract	The mouse Clock gene encodes a basic helix–loop–helix-PAS transcription factor, CLOCK, that acts in concert with BMAL1 to form the positive elements of the circadian clock mechanism in mammals. The original Clock mutant allele is a dominant negative (antimorphic) mutation that deletes exon 19 and causes an internal deletion of 51 aa in the C-terminal activation domain of the CLOCK protein. Here we report that heterozygous Clock/+ mice exhibit high-amplitude phase-resetting responses to 6-h light pulses (Type 0 resetting) as compared with wild-type mice that have low amplitude (Type 1) phase resetting. The magnitude and time course of acute light induction in the suprachiasmatic nuclei of the only known light-induced core clock genes, Per1 and Per2, are not affected by the Clock/+ mutation. However, the amplitude of the circadian rhythms of Per gene expression are significantly reduced in Clock homozygous and heterozygous mutants. Rhythms of PER2::LUCIFERASE expression in suprachiasmatic nuclei explant cultures also are reduced in amplitude in Clock heterozygotes. The phase–response curves to changes in culture medium are Type 0 in Clock heterozygotes, but Type 1 in wild types, similar to that seen for light in vivo. The increased efficacy of resetting stimuli and decreased PER expression amplitude can be explained in a unified manner by a model in which the Clock mutation reduces circadian pacemaker amplitude in the suprachiasmatic nuclei.
Related Links	http://dx.doi.org/10.1073/pnas.0603601103
Ending Page	9332
Page Count	6
Starting Page	9327
File Format	PDF
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	24
Volume Number	103
Language	English
Publisher	National Academy of Sciences
Publisher Date	2006-06-13
Access Restriction	Open
Rights Holder	National Academy of Sciences
Subject Keyword	General Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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