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在Clock突变小鼠的视交叉上核中,Dec1和Dec2的表达受到破坏。

Dec1 and Dec2 expression is disrupted in the suprachiasmatic nuclei of Clock mutant mice.

作者信息

Butler Matthew Preston, Honma Sato, Fukumoto Tatsuya, Kawamoto Takeshi, Fujimoto Katsumi, Noshiro Mitsuhide, Kato Yukio, Honma Ken-ichi

机构信息

Department of Physiology, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan.

出版信息

J Biol Rhythms. 2004 Apr;19(2):126-34. doi: 10.1177/0748730403262870.

Abstract

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 time-dependent 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.

摘要

DEC1和DEC2是碱性螺旋-环-螺旋转录因子,在功能上类似于哺乳动物生物钟的负反馈成分。Dec1和Dec2基因在大鼠视交叉上核中有节律地表达,并且Dec1的表达以一种即时早期基因的动力学方式被光以时间依赖性方式刺激。DEC1和DEC2可以抑制生物钟基因Per1的CLOCK:BMAL1反式激活,这表明这些转录因子可能有助于调节昼夜节律时间。作者展示了野生型和纯合Clock突变小鼠中Dec1和Dec2的表达模式数据。在视交叉上核中,Clock突变显著降低了Dec1和Dec2的表达。Dec1变得无节律;Dec2在12小时光照:12小时黑暗的光暗循环中仍有微弱节律,但在持续黑暗中无节律。在所有检测的脑区中均检测到Clock突变小鼠中Dec1和Dec2信号的显著减弱。这些数据表明Clock在体内对Dec1和Dec2有上调作用。

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