The molecular players of circadian clock oscillation have been identified and extensively characterized. The epigenetic mechanisms behind the circadian gene expression control has also been recently studied, although there are still details to be illucidated. In this review, we briefly summarize the current understanding of the mammalian clock. We also provide evidence for the lack of circadian oscillation in particular cell types. As the circadian clock has intimate interaction with the various cellular functions in different type of cells, it must have plasticity and specicity in its operation within different epigenetic environments. The lack of circadian oscillation in certain cells provide an unique opportunity to study the required epigenetic environment in the cell that permit circadian oscillation and to idenfify key influencing factors for proper clock function. How epigenetic mechansims, including DNA methylaiton and chromatin modifications, participate in control of clock oscillation still awaits future studies at the genomic scale. 1. Introduction Mammals have overt circadian rhythms in their physiology and behavior, orchestrated by the suprachiasmatic nucleus of the anterior hypothalamus [1, 2]. The endogenous circadian clock enables organisms to anticipate the regular daily changes in the environment and temporally organize their life activities [3, 4]. Fundamentally, circadian timing functions exist at the cellular level not only for suprachiasmatic neurons, but also for cells of various peripheral tissues [5–9]. 2. A Brief Overview of Clockwork Mechanisms The past two decades witnessed the rapid pace in gaining in-depth understanding of mammalian clockwork operation. Circadian oscillations are generated at the molecular level by a set of clock genes [10–12]. The mapping and cloning of the ClockΔ19 mutation through ENU mutagenesis and positional cloning set the stage for elucidation of mammalian clockwork mechanisms [13–15]. BMAL1 was soon identified to be the dimerization partner of CLOCK to drive clock gene expression [16, 17]. Mouse Per genes were also identified and found to be driven by the CLOCK/BMAL1 dimer [18–20]. CRY1 and CRY2 were later found to have essential roles in the integrity of the circadian clock through inhibiting CLOCK/BMAL1-mediated transcription activation [21, 22]. Thus CLOCK and BMAL1 form the positive limb, while CRY and PER proteins form the negative limb of the transcriptional feedback loop [23]. Later on, more details were elucidated and revisions were made for the clockwork model, including the antagonistic
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