CALCIUM/CALMODULIN-DEPENDENT PROTEIN-KINASE-II AND POTASSIUM CHANNEL SUBUNIT EAG SIMILARLY AFFECT PLASTICITY IN DROSOPHILA
CALCIUM/CALMODULIN-DEPENDENT PROTEIN-KINASE-II AND POTASSIUM CHANNEL SUBUNIT EAG SIMILARLY AFFECT PLASTICITY IN DROSOPHILA
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DOI：
10.1073/pnas.91.21.10044
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发表时间：
1994-10-11
影响因子：
11.1
通讯作者：
GREENSPAN, RJ
中科院分区：
文献类型：
--
作者：
GRIFFITH, LC;WANG, J;GREENSPAN, RJ
在黑腹果蝇中，通过抑制钙/钙调蛋白依赖性蛋白激酶II和钾通道亚基基因eag的突变，产生了突触传递和联想学习的类似缺陷。这些行为和突触缺陷在同时携带eag突变和蛋白激酶抑制剂转基因的动物中并不是简单的叠加，这增加了这些表型共享共同途径的可能性。在分子水平上，Eag的一部分推定的胞质结构域是钙/钙调蛋白依赖性蛋白激酶II的底物。这些相似性的行为和突触生理学，遗传相互作用，并在体外的两个分子的生化相互作用表明，神经和行为的可塑性的一个重要组成部分可能是介导的fag功能的钙/钙调蛋白依赖性蛋白激酶II的调制。
Similar defects in both synaptic transmission and associative learning are produced in Drosophila melanogaster by inhibition of calcium/calmodulin-dependent protein kinase II and mutations in the potassium channel subunit gene eag. These behavioral and synaptic defects are not simply additive in animals carrying both an eag mutation and a transgene for a protein kinase inhibitor, raising the possibility that the phenotypes share a common pathway. At the molecular level, a portion of the putative cytoplasmic domain of Eag is a substrate of calcium/calmodulin-dependent protein kinase II. These similarities in behavior and synaptic physiology, the genetic interaction, and the in vitro biochemical interaction of the two molecules suggest that an important component of neural and behavioral plasticity may be mediated by modulation of fag function by calcium/calmodulin-dependent protein kinase II.