A congenital heart defect in Drosophila caused by an action-potential mutation
A congenital heart defect in Drosophila caused by an action-potential mutation
复制标题
DOI：
10.3109/01677069509083461
复制
发表时间：
1995-01-01
影响因子：
1.9
通讯作者：
White, L
中科院分区：
文献类型：
--
作者：
Dowse, H;Ringo, J;White, L
突变无动作电位（温度敏感）（nap（ts））在温度高于20摄氏度时诱导黑腹果蝇幼虫的心跳心律失常;心跳在回到20摄氏度后再次恢复正常节律。对于这种表型，nap（ts）对野生型几乎完全隐性。NAP（TS）还在很宽的温度范围内降低心率的温度敏感性，对于这种表型，NAP（TS）相对于野生型是显性的，NAP（TS）通过对麻痹（TS）（一种编码电压依赖性钠通道的基因）的表达的上位效应在成人中引起可逆的麻痹。然而，帕拉（tsl）突变在29摄氏度时会导致成虫瘫痪，但在20摄氏度至37.5摄氏度的温度下对幼虫的心跳没有影响。与早先的报道相反，经期基因对心跳没有影响。
The mutation no action potential(temperature sensitive) (nap(ts)) induces arrhythmia in the heartbeat of Drosophila melanogaster larvae at temperatures above 20 degrees C; heartbeat becomes normally rhythmic again after a shift back to 20 degrees C. For this phenotype, nap(ts) is almost completely recessive to the wild type. nap(ts) also reduces the temperature-sensitivity of heart rate over a wide range of temperatures, for this phenotype, nap(ts) is dominant over the wild type, nap(ts) causes reversible paralysis in adults by epistatic effects on the expression of paralytic(ts), a gene encoding a voltage-dependent sodium channel. However, the para(tsl) mutation, which induces paralysis in adults at 29 degrees C, has no effect on larval heartbeat at temperatures between 20 degrees and 37.5 degrees C. The period gene, contra earlier reports, has no effect on heartbeat.