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Comment
. 2007 Jun 5;104(23):9553-4.
doi: 10.1073/pnas.0703516104. Epub 2007 May 29.

Lean gene and the clock machine

Kathryn Moynihan Ramsey  1 , Joseph Bass
Affiliations
Comment

Lean gene and the clock machine

Kathryn Moynihan Ramsey et al. Proc Natl Acad Sci U S A. .
No abstract available

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Conflict of interest statement

Conflict of interest statement: J.B. has been a consultant for Amylin, Genentech, Merck, and Takeda Pharmaceuticals.

Figures

Fig. 1.
Fig. 1.
Emerging studies continue to identify core elements and the physiologic functions of the intrinsic molecular oscillator. (A) Core molecular clock machinery. CLOCK/NPAS2 (circadian locomotor output cycles kaput/neuronal PAS domain protein 2) and BMAL1 (brain and muscle ARNT-like 1) constitute the positive limb of the core circadian network by activating downstream targets, including the period (Per), cryptochrome (Cry), Ror, and Rev-Erb genes. The major negative limb of the circadian network is mediated by PER and CRY, which inhibit CLOCK/BMAL1 activity. CK1ε/δ (casein kinases I ε and δ) phosphorylates PER and CRY and triggers the degradation of PER, and the RORs and REV-ERBs, circadian-controlled metabolic transcription factors, regulate Bmal1 transcription. (B) Integration of molecular clock and metabolic systems. Both direct and indirect transcriptional targets of the clock machinery participate in regulation of energy balance and metabolism at multiple levels within both the CNS and peripheral tissues. The CNS clock output involves signaling from the central pacemaker neurons of the suprachiasmatic nucleus (SCN), which synchronizes clock gene expression within extra-SCN regions of the brain and many peripheral metabolic tissues. Transcription of Nocturnin, a well characterized deadenylase, is highly rhythmic in several peripheral tissues and has now been identified as an important factor modulating the response to diet-induced obesity.
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