A molecular mechanism regulating rhythmic output from the suprachiasmatic circadian clock.

TL;DR: The identification of a group of genes that are believed to constitute the molecular core of the circadian clock in the retina, although with a slightly different 24-h profile from that observed in the central circadian pacemaker, suggests that some difference may exist between the retinal clock and the clock located in the suprachiasmatic nuclei of hypothalamus.

TL;DR: The experiments find a new regulator for circadian clock at the post-translational level and demonstrate a different regulatory function for the circadian clock through the deubiquitination and the up-regulation of the core clock protein BMAL1 in the positive limb of the transcription-translation feedback loop.

TL;DR: The data suggest that activator protein-1 binding sites on ventrolateral suprachiasmatic nucleus target genes are constitutively occupied by DeltaFosB/JunD complexes, and that c-Fos, Fra-2, FosB and JunB compete for binding after photic stimulation.

TL;DR: Comparisons and differences in the molecular mechanisms of the clock machinery between the primary SCN clock and extra-SCN brain clocks are presented to raise the possibility that pathophysiological alterations of internal timing that are deleterious for health may result from internal desynchronization within the network of cerebral clocks.

TL;DR: The power of ENU mutagenesis combined with the ability to clone murine genes by map position provides a generally applicable approach to study complex behavior in mammals.

TL;DR: It is suggested that the SCN contains a large population of autonomous, single-cell circadian oscillators, and that synapses formed in vitro are neither necessary for operation of these oscillators nor sufficient for synchronizing them.

TL;DR: CLOCK represents the second example of a PAS domain-containing clock protein (besides Drosophila PERIOD), which suggests that this motif may define an evolutionarily conserved feature of the circadian clock mechanism.

TL;DR: The dominant late elongated hypocotyl (lhy) mutation of Arabidopsis disrupted circadian clock regulation of gene expression and leaf movements and caused flowering to occur independently of photoperiod.