Intracellular Ca2+ regulates free-running circadian clock oscillation in vivo

被引:106
作者
Harrisingh, Marie C.
Wu, Ying
Lnenicka, Gregory A.
Nitabach, Michael N.
机构
[1] Yale Sch Med, Dept Cellular & Mol Physiol, New Haven, CT 06520 USA
[2] SUNY Albany, Dept Biol Sci, Albany, NY 12222 USA
关键词
Ca2+; circadian rhythm; Drosophila; calmodulin; CaMKII; transcription;
D O I
10.1523/JNEUROSCI.3680-07.2007
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Although circadian oscillation in dynamics of intracellular Ca2+ signals has been observed in both plant and animal cells, it has remained unknown whether Ca2+ signals play an in vivo role in cellular oscillation itself. To address this question, we modified the dynamics of intracellular Ca2+ signals in circadian pacemaker neurons in vivo by targeted expression of varying doses of a Ca2+ buffer protein in transgenic Drosophila melanogaster. Intracellular Ca2+ buffering in pacemaker neurons results in dose-dependent slowing of free-running behavioral rhythms, with average period >3 h longer than control at the highest dose. The rhythmic nuclear accumulation of a transcription factor known to be essential for cellular circadian oscillation is also slowed. We also determined that Ca2+ buffering interacts synergistically with genetic manipulations that interfere with either calmodulin or calmodulin-dependent protein kinase II function. These results suggest a role for intracellular Ca2+ signaling in regulating intrinsic cellular oscillation in vivo.
引用
收藏
页码:12489 / 12499
页数:11
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