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Light does not degrade the constitutively expressed BMAL1 protein in the mouse suprachiasmatic nucleus by Charlotte Von Gall; Elizabeth Noton; Choogon Lee; David R. Weaver is a Neuroscience article available to read on EtoBox.

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## Abstract Biological rhythms in mammals are driven by a central circadian clock located in the suprachiasmatic nucleus (SCN). At the molecular level the biological clock is based on the rhythmic expression of clock genes. Two basic helix–loop–helix (bHLH)/PAS‐containing transcription factors, CLOCK and BMAL1 (MOP3), provide the basic drive to the system by activating transcription of negative regulators through E box enhancer elements. A critical feature of circadian timing is the ability of the clockwork to be entrained to the environmental light/dark cycle. The light‐resetting mechanism of the mammalian circadian clock is poorly understood. Light‐induced phase shifts are correlated with the induction of the clock genes __mPer1__ and __mPer2__ and a subsequent increase in mPER1 protein levels. It has previously been suggested that rapid degradation of BMAL1 protein in the rat SCN is part of the resetting mechanism of the central pacemaker. Our study shows that BMAL1 and CLOCK proteins are continuously expressed at high levels in the mouse SCN, supporting the hypothesis that rhythmic negative feedback plays the major role in rhythm generation in the mammalian pacemaker. Using bot

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Author

Charlotte Von Gall; Elizabeth Noton; Choogon Lee; David R. Weaver

Publisher

John Wiley and Sons; Wiley (Blackwell Publishing); Blackwell Publishing Inc.; Wiley (ISSN 0953-816X)

Published

2003

Language

EN

Field

Neuroscience (Life Sciences)