Dec1 and Dec2 Expression is Disrupted in the Suprachiasmatic Nuclei of Clock Mutant Mice

DOI Web Site 被引用文献4件
  • Matthew Preston Butler
    Department of Physiology, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan
  • Sato Honma
    Department of Physiology, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan,
  • Tatsuya Fukumoto
    Department of Physiology, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan
  • Takeshi Kawamoto
    Department of Dental and Medical Biochemistry, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8553, Japan
  • Katsumi Fujimoto
    Department of Dental and Medical Biochemistry, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8553, Japan
  • Mitsuhide Noshiro
    Department of Dental and Medical Biochemistry, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8553, Japan
  • Yukio Kato
    Department of Dental and Medical Biochemistry, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8553, Japan
  • Ken-Ichi Honma
    Department of Physiology, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan

抄録

<jats:p> DEC1 and DEC2 are basic helix-loop-helix transcription factors that functionally resemble negative feedback components of the mammalian circadian clock. The genes Dec1 and Dec2 are expressed rhythmically in the rat suprachiasmatic nuclei, and Dec1 expression is stimulated by light in a timedependent manner with the kinetics of an immediate early gene. DEC1 and DEC2 can inhibit CLOCK:BMAL1 transactivation of the clock gene Per1, suggesting that these transcription factors may help regulate circadian timing. The authors present data on the expression pattern of Dec1 and Dec2 in wild-type and homozygous Clock mutant mice. In the suprachiasmatic nuclei, the Clock mutation significantly reduces the expression of Dec1 and Dec2. Dec1 becomes arrhythmic; Dec2 remains weakly rhythmic in a 12L:12D light-dark cycle but is arrhythmic in constant darkness. A robust attenuation of the Dec1 and Dec2 signals in Clock mutant mice was detected in all brain areas examined. These data point to up-regulation of Dec1 and Dec2 by Clock in vivo. </jats:p>

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