The mouse Clock mutation reduces circadian pacemaker amplitude and enhances efficacy of resetting stimuli and phase-response curve amplitude.

The mouse Clock mutation reduces circadian pacemaker amplitude and enhances efficacy of resetting stimuli and phase-response curve amplitude. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

The mouse Clock mutation reduces circadian pacemaker amplitude and enhances efficacy of resetting stimuli and phase-response curve amplitude. Abstract Text:

Martha Hotz Vitaterna,Caroline H Ko,Anne-Marie Chang,Ethan D Buhr,Ethan M Fruechte,Andrew Schook,Marina P Antoch,Fred W Turek,Joseph S Takahashi,

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.

The mouse Clock mutation reduces circadian pacemaker amplitude and enhances efficacy of resetting stimuli and phase-response curve amplitude. Publishing Authors By Initials

MH Vitaterna,CH Ko,AM Chang,ED Buhr,EM Fruechte,A Schook,MP Antoch,FW Turek,JS Takahashi,

For similar proteins: transcription factors research abstracts see: proteins: transcription factors research

PUBMED ID PMID:

MEDLINE DATE:

The mouse Clock mutation reduces circadian pacemaker amplitude and enhances efficacy of resetting stimuli and phase-response curve amplitude. Journal Published:

PUBLICATION TYPE: Research Support, U.S. Gov't,

Journal: Proceedings of the National Academy of Sciences of

VOLUME: 103

Page Numbers: 9327-32

Journal Abbreviation: Proc. Natl. Acad. Sci. U.S.A.

ISSN: 0027-8424

DAY: 5

MONTH: 06

YEAR: 2006

The mouse Clock mutation reduces circadian pacemaker amplitude and enhances efficacy of resetting stimuli and phase-response curve amplitude. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 7505876

The mouse Clock mutation reduces circadian pacemaker amplitude and enhances efficacy of resetting stimuli and phase-response curve amplitude. Keywords Mesh Terms:

KEYWORDS: Transcription Factors

MESH TERMS: metabolism

Chemical & Substance for Abstract: The mouse Clock mutation reduces circadian pacemaker amplitude and enhances efficacy of resetting stimuli and phase-response curve amplitude. Information

Substance Name: Transcription Factors

Registry Number: 0

Grant and Affiliation Information for The mouse Clock mutation reduces circadian pacemaker amplitude and enhances efficacy of resetting stimuli and phase-response curve amplitude.

AFFILIATION: Center for Functional Genomics, Center for Sleep and Circadian Biology and Department of Neurobiology and Physiology, Northwestern University, 2205 Tech Drive, Evanston, IL 60208-3520, USA.

Country: United States

AGENCY: United States NIMH

GRANT: U01 MH61915

ACRONYM: MH

MEDLINETA: Proc Natl Acad Sci U S A

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

The mouse Clock mutation reduces circadian pacemaker amplitude and enhances efficacy of resetting stimuli and phase-response curve amplitude Related Publications

• A noncanonical E-box enhancer drives mouse Period2 circadian oscillations in vivo.
• Bone morphogenetic protein 2 stimulates osteoclast differentiation and survival supported by receptor activator of nuclear factor-kappaB ligand.
• Circadian rhythms: the cancer connection.
• Comparison between stabilometry with and without head tilts in a roll plane.
• Effect of Escherichia coli wild type or its derivative with high nitrite reductase activity on in vitro ruminal methanogenesis and nitrate/nitrite reduction.
• Effect of gravity on apical dominance in Pharbitis nil.
• Effect of oral branched chain amino acid-rich nutrient administered during endoscopic injection sclerotherapy of cirrhotic patients.
• Forward genetic screens to identify circadian rhythm mutants in mice.
• Genome-wide epistatic interaction analysis reveals complex genetic determinants of circadian behavior in mice.
• Identification of the cDNA of differentially expressed genes in the transition zone of cucumber seedlings by fluorescent differential display.
• In vivo bone-forming capacity of human bone marrow-derived stromal cells is stimulated by recombinant human bone morphogenetic protein-2.
• Isolation of auxin efflux carrier cDNA from cucumber.
• Methods to record circadian rhythm wheel running activity in mice.
• Mice lacking smooth muscle calponin display increased bone formation that is associated with enhancement of bone morphogenetic protein responses.
• Mouse chimeras and their application to circadian biology.
• Novel hydrotropism mutants of Arabidopsis thaliana and their altered waving response and phototropism.
• Oral myiasis treated with ivermectin: case report.
• Osteoblasts provide a suitable microenvironment for the action of receptor activator of nuclear factor-kappaB ligand.
• Osteoprotegerin regulates bone formation through a coupling mechanism with bone resorption.
• Pax 2 expression in mesodermal segmentation and its relationship with EphA4 and Lunatic-fringe during chicken somitogenesis.
• Physiological and genetic characterization of hydrotropic mutants of Arabidopsis thaliana.
• Real-time luminescence reporting of circadian gene expression in mammals.
• Regulations: what next?
• The effect of light on the gravimorphogenesis of cucumber seedlings.
• The mouse Clock mutation reduces circadian pacemaker amplitude and enhances efficacy of resetting stimuli and phase-response curve amplitude.
• [Bone morphogenetic protein (BMP): from basic studies to clinical approaches]
• [Differential expression of a homing-related molecule repertoire among umbilical cord blood, mobilized peripheral blood and bone marrow-derived hematopoietic stem/progenitor cells.]
• [Gravitaxis of paramecium: testing the hypotheses by free-fall experiments]
• [Sequence variability in Borna disease virus ORF II from human beings]
• [The effects of space environment on differentiation and mutation frequency in Dictyostelium discoideum]