Mop3 is an essential component of the master circadian pacemaker in mammals

Article Abstract:

Results support a genetic role of MOP3 as a genuine heterodimeric partner of the molecular clock in mammals. Data show that the elimination of MOP3 abolishes circadian rhythmicity and impairs locomotor activity suggesing that origin of such phenotypes is due to loss of circadian function.

United States, Statistical Data Included, Analysis, Physiological regulation, Gene expression, Mammals, Locomotion

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Positional cloning of the mouse circadian Clock gene

Article Abstract:

The circadian clock (Clock) gene in mice was identified via a forward genetic approach involving single-gene mutations. Northern blot analysis indicated the localized expression of the Clock gene in the hypothalamus and eyes which contained self-sustaining circadian oscillators. Mutations in the novel circadian clock gene also increased the duration of the circadian period in mutants compared to wild-type strains. Furthermore, the Clock gene was characterized as the master regulator of the circadian pacemaker function by controlling the expression patterns of the circadian oscillator.

Mice as laboratory animals, House mouse

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Functional identification of the mouse circadian Clock gene by transgenic BAC rescue

Article Abstract:

The molecular mechanisms of circadian rhythms in mice was analyzed based on a forward genetic approach involving phenotype-driven N-ethyl-N-nitrosourea (ENU) mutagenesis. Analysis of Clock mutation complementation in transgenic mice that were constructed from a set of overlapping bacterial artificial chromosome clones indicated the presence of a large transcription unit that encoded a basic-helix-loop-helix-PAS domain protein. Furthermore, the integral circadian pacemaking system was altered by the overexpression of the Clock gene.

Genetically modified mice

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