LOSS OF CALCIUM CALMODULIN RESPONSIVENESS IN ADENYLATE-CYCLASE OF RUTABAGA, A DROSOPHILA LEARNING MUTANT
LOSS OF CALCIUM CALMODULIN RESPONSIVENESS IN ADENYLATE-CYCLASE OF RUTABAGA, A DROSOPHILA LEARNING MUTANT
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DOI：
10.1016/0092-8674(84)90316-7
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发表时间：
1984-01-01
期刊：
影响因子：
64.5
通讯作者：
QUINN, WG
中科院分区：
文献类型：
--
作者：
LIVINGSTONE, MS;SZIBER, PP;QUINN, WG
一个X连锁的隐性突变被分离出来，并在果蝇中定位，阻止联想学习，它的部分特点是生化。该突变影响腺苷酸环化酶活性。突变苍蝇的环化酶活性不同于野生型酶，因为它不受钙或钙调素的刺激。突变环化酶活性确实对鸟苷酸、氟化物和单胺有反应，这表明该缺陷既不存在于激素受体中，也不存在于已知的GTP结合调节蛋白中。该突变可能直接影响催化亚基。显然，至少有一种其他类型的腺苷酸环化酶活性不受突变的影响，对Ca/钙调素不敏感。
An X-linked recessive mutation was isolated and mapped in Drosophila that blocks associative learning, and it was partially characterized biochemically. The mutation affects adenylate cyclase activity. Cyclase activity from mutant flies differed from the wild-type enzyme in that it was not stimulated by Ca or calmodulin. Mutant cyclase activity did respond to guanyl nucleotides, fluoride and monoamines, which suggests that the defect is neither in the hormone receptor nor in either known GTP-binding regulatory protein. The mutation possibly affects the catalytic subunit directly. Apparently, there is at least one other type of adenylate cyclase activity that is unaffected by the mutation and insensitive to Ca/calmodulin.