Compression of daily activity time in mice lacking functional Per or Cry genes. (June 2014)

• Record Type: Journal Article
• Authors: Spoelstra, K.; Comas, M.; Daan, S.
• Is Part Of: Chronobiology international. Volume 31:Number 5(2014)
• Page Start: 645
• Page End: 654
• Publication Date: 2014-06
• Subjects: Chronobiology -- Periodicals; Biological rhythms -- Periodicals; Circadian rhythms -- Periodicals; 571.77
• DOI: 10.3109/07420528.2014.885529
• Languages: English
• ISSNs: 0742-0528

Abstract

<abstract> <title> <x xml:space="preserve">Abstract</x> </title> <p>The adjustment of daily activity time (α) to the varying night length in nocturnal creatures was one of the functions originally attributed to a putative dual oscillator structure of circadian pacemakers in mammals. In two experimental approaches, we tested whether this ability is compromised in mice with functional deletions of one of the four circadian clock genes. First, we tested the capability of α compression by long days in <italic>mPer1<sup>Brdm1</sup></italic> and <italic>mPer2<sup>Brdm1</sup></italic> mutant mice. When exposed to a full L:D 18:6 photoperiod, wild-type and <italic>mPer1<sup>Brdm1</sup></italic> mutant mice show compression followed by decompression of α in DD. <italic>mPer2<sup>Brdm1</sup></italic> mutant mice did not compress their activity time. The interpretation of these data is, however, complicated by masking due to light. We, therefore, embarked on a second experiment, exploiting skeleton photoperiods. The skeleton photoperiod was changed stepwise from 0 to 24 h, and <italic>mCry1</italic> and <italic>mCry2</italic> knockout mice were now included in the design. We observed clear and systematic compression of α in wild-type and <italic>mCry1</italic> and <italic>mCry2</italic> knockout mice. <italic>mPer1<sup>Brdm1</sup></italic> and <italic>mPer2<sup>Brdm1</sup></italic> mice both poorly entrained to the skeleton photoperiod. The single <italic>mPer2<sup>Brdm1</sup></italic> mutant mouse that did entrain did not show α compression. The results show that neither <italic>mCry1</italic> nor <italic>mCry2</italic> deletions compromise adjustment to day length, consistent with our earlier conclusions on period lengthening in constant light (Spoelstra & Daan, 2008). The <italic>mPer2<sup>Brdm1</sup></italic> mutant behaves aberrantly and appears not to respond to the delaying action of light in the late subjective day.</p> </abstract>