Photic induction of mPer1 and mPer2 in Cry-deficient mice lacking a biological clock
Photic induction of mPer1 and mPer2 in Cry-deficient mice lacking a biological clock
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DOI：
10.1126/science.286.5449.2531
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发表时间：
1999-12-24
期刊：
影响因子：
56.9
通讯作者：
van der Horst, GTJ
中科院分区：
文献类型：
--
作者：
Okamura, H;Miyake, S;van der Horst, GTJ
缺乏mCry1和mCry2的小鼠行为不规律。如图所示，时钟基因mPer1和mPer2（哺乳动物周期基因1和2）在视交叉上核和外周组织中的循环表达被消除，mPer1和mPer2的mRNA水平构成性地高。这些发现表明，在缺乏mCRY1和mCRY2（哺乳动物隐色素1和2）的情况下，生物钟被消除，并支持哺乳动物CRY蛋白在昼夜节律反馈回路负肢中起作用的观点。mCry双突变小鼠在短暂的光刺激下保留了mPer1和mPer2表达的能力，这种光刺激可以使野生型动物的生物钟相移。因此，mCRY1和mCRY2对于光诱导的生物钟相移是不可缺少的。
Mice Lacking mCry1 and mCry2 are behaviorally arrhythmic. As shown here, cyclic expression of the clock genes mPer1 and mPer2 (mammalian Period genes 1 and 2) in the suprachiasmatic nucleus and peripheral tissues is abolished and mPer1 and mPer2 mRNA Levels are constitutively high. These findings indicate that the biological clock is eliminated in the absence of both mCRY1 and mCRY2 (mammalian cryptochromes 1 and 2) and support the idea that mammalian CRY proteins act in the negative Limb of the circadian feedback Loop. The mCry double-mutant mice retain the ability to have mPer1 and mPer2 expression induced by a brief Light stimulus known to phase-shift the biological clock in wild-type animals. Thus, mCRY1 and mCRY2 are dispensable for Light-induced phase shifting of the biological clock.