Levin L R, Han P L, Hwang P M, Feinstein P G, Davis R L, Reed R R
Howard Hughes Medical Institute, Johns Hopkins School of Medicine, Baltimore, Maryland 21205.
Cell. 1992 Feb 7;68(3):479-89. doi: 10.1016/0092-8674(92)90185-f.
Four putative adenylyl cyclase genes from Drosophila melanogaster were identified by virtue of their extensive sequence homology with mammalian cyclases. One corresponds to the learning and memory gene rutabaga and is most similar to the mammalian brain Ca2+/calmodulin (CaM)-responsive cyclase. In a mammalian expression system, rutabaga cyclase activity was stimulated approximately 5-fold by the presence of Ca2+/CaM. A point mutation, identified at this locus in rut1 mutant flies, resulted in loss of detectable adenylyl cyclase activity. New P element insertion-induced rutabaga mutations mapped to within 200 nucleotides of the 5' end of the rutabaga cDNA. These data confirm the identity of the rutabaga locus as the structural gene for the Ca2+/CaM-responsive adenylyl cyclase and show that the inactivation of this cyclase leads to a learning and memory defect.
通过与哺乳动物环化酶的广泛序列同源性,鉴定出了来自黑腹果蝇的四个假定的腺苷酸环化酶基因。其中一个与学习和记忆基因芜菁甘蓝相对应,并且与哺乳动物脑Ca2+/钙调蛋白(CaM)反应性环化酶最为相似。在哺乳动物表达系统中,Ca2+/CaM的存在使芜菁甘蓝环化酶活性大约提高了5倍。在rut1突变果蝇的这个位点鉴定出的一个点突变,导致可检测到的腺苷酸环化酶活性丧失。新的P因子插入诱导的芜菁甘蓝突变定位于芜菁甘蓝cDNA 5'端的200个核苷酸范围内。这些数据证实了芜菁甘蓝位点作为Ca2+/CaM反应性腺苷酸环化酶结构基因的身份,并表明这种环化酶的失活导致学习和记忆缺陷。