Long-Term Constant Light Induces Constitutive Elevated Expression of mPER2 Protein in the Murine SCN: A Molecular Basis for Aschoff’s Rule?

Jan 18, 2005Journal of biological rhythms

Long-term constant light causes continuous high levels of a key clock protein in the mouse brain's daily rhythm center, supporting Aschoff's rule

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Abstract

Under long-term light exposure, mPER2 levels are elevated and consistently expressed in the SCN.

Clock genes mPer1, mPer2, mCry1, and mCry2 maintain rhythmic expression in long-term light conditions, although mCry2's waveform changes.
Rhythmic protein levels of mPER1, mCRY1, and mCRY2 under long-term light are similar to those observed in dark conditions.
mPER2 is expressed at elevated levels under long-term light, indicating a role in phase delays of the molecular clock.
The rhythmic expression of other clock genes does not rely on the rhythmic production of mPER2.
These findings suggest that long-term light exposure lengthens the circadian period by preventing the decline of mPER2.

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Circadian rhythms in behavior, metabolism, and physiology are based upon transcriptional/translational feedback loops involving a core set of clock genes that interact to regulate their own expression. In mammals, the SCN is the site of a master biological clock regulating circadian locomotor rhythms. The products of the clock genes mPer1, mPer2, mCry1, and mCry2 form essential components of both negative and positive elements within the SCN oscillator. The primary aims of this study were to examine clock gene abundance under longterm LL in an attempt to provide molecular correlates of the lengthened tau and daily phase delays described by Aschoff's rule. Wheel-running behavior was recorded from mice maintained in either DD or LL for 50 days. The abundance of the clock genes mPer1, mPer2, mCry1, and mCry2 and their protein products was then examined (every approximately 4 h) within the SCN using in situ hybridization and immunocytochemistry. Under LL conditions, mPer1, mPer2, mCry1, and mCry2 messages remained rhythmic, although the waveform of mCry2 was altered compared to DD. In LL, mPER1, mCRY1, and mCRY2 protein levels were also rhythmic and comparable to the patterns observed in DD. However, mPER2 is elevated and constitutively expressed under LL. Thus, rhythmic expression of these clock genes is not dependent on the rhythmic production of mPER2, and the acute up-regulation of mPer1 and mPer2 described for short (nonparametric) light pulses is not sustained under LL conditions. These findings suggest that mPER2 is important for the generation of phase delays in the molecular clockwork, providing a possible molecular explanation for Aschoff's rule: LL lengthens the circadian period by inhibiting the degeneration of mPER2, and constitutively elevated levels of mPER2 enhance the phase-delaying limb of the molecular oscillator.

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Long-Term Constant Light Induces Constitutive Elevated Expression of mPER2 Protein in the Murine SCN: A Molecular Basis for Aschoff’s Rule?

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