Martin J R, Ollo R
Institut Pasteur, Paris, France.
EMBO J. 1996 Apr 15;15(8):1865-76.
Calcium/calmodulin-dependent protein kinases (CaM kinases) have been reported to be involved in neuroplasticity. We have cloned a new Drosophila CaM kinase gene named caki. We describe the molecular characterization of caki and a behavioral effect of its elimination. The caki gene is extremely large; comparison of the genomic and cDNA sequences reveals that the caki transcription unit is at least 150 kb. The catalytic domain of this new CaM kinase protein shares homology (41%) with type II CaM kinases, while the C-terminal part is divergent. Constitutively expressed Caki protein is enzymatically active since it causes a 3-fold increase in the level of the Rous sarcoma virus long terminal repeat (RSV LTR) promoter in a co-transfusion assay. In situ hybridization shows that during embryogenesis, larval and pupal life, transcription of caki is restricted almost exclusively to the central nervous system. In the adult head, immunohistochemistry reveals Caki protein in the lamina, the neuropil of the medulla, lobula, lobula plate and in the central brain. Mutant caki flies show reduced walking speed in 'Buridan's paradigm'.
据报道，钙/钙调蛋白依赖性蛋白激酶（CaM激酶）参与神经可塑性。我们克隆了一个名为caki的新果蝇CaM激酶基因。我们描述了caki的分子特征及其缺失所产生的行为效应。caki基因非常大；基因组和cDNA序列比较显示，caki转录单位至少为150 kb。这种新的CaM激酶蛋白的催化结构域与II型CaM激酶具有同源性（41%），而其C末端部分则有所不同。组成型表达的Caki蛋白具有酶活性，因为在共转染试验中，它会使劳斯肉瘤病毒长末端重复序列（RSV LTR）启动子水平增加3倍。原位杂交显示，在胚胎发育、幼虫和蛹期，caki的转录几乎完全局限于中枢神经系统。在成年果蝇头部，免疫组织化学显示在神经层、髓质神经纤维网、小叶、小叶板和中枢脑中存在Caki蛋白。突变的caki果蝇在“布里丹范式”中行走速度降低。
