Smith R F, Konopka R J
Mol Gen Genet. 1981;183(2):243-51. doi: 10.1007/BF00270625.
The circadian rhythm phenotypes of eight chromosome aberrations with a breakpoint in the region of the per locus (3B1-2) were analyzed. Two duplications and five deficiencies with a 3B1-2 breakpoint produce either a wild-type or an arrhythmic clock phenotype while one translocation with a 3B1-2 breakpoint. T(1;4)JC43, produces locomotor-activity rhythms with either very-long period (31--39 h), rhythms that grade into arrhythmicity, or completely arrhythmic phenotypes. This is a unique phenotype that had not previously been observed for mutants at the per locus. An extensive complementation analysis of 3B1-2 chromosome aberrations and per mutant alleles provided no compelling evidence for genetic complexity at the per locus. This is in contrast to the report of Young and Judd (1978). Analysis of both the locomotor-activity and eclosion phenotypes of 3B1-2 chromosome aberrations did not uncover differences in the genetic control of these two rhythms. The clock phenotypes of 3B1-2 chromosome aberrations, the three per mutant alleles, and per+ duplications suggest that mutations at the per locus shorten, lengthen, or eliminate periodicity by respectively increasing, decreasing, or eliminating per activity.
分析了8种染色体畸变在周期素基因座（3B1-2）区域有断点时的昼夜节律表型。两个在3B1-2有断点的重复和五个缺失产生野生型或无节律的时钟表型，而一个在3B1-2有断点的易位，即T(1;4)JC43，产生的运动活动节律具有极长周期（31-39小时）、逐渐变为无节律或完全无节律的表型。这是一种以前在周期素基因座的突变体中未观察到的独特表型。对3B1-2染色体畸变和周期素突变等位基因进行的广泛互补分析，没有提供关于周期素基因座遗传复杂性的令人信服的证据。这与扬和贾德（1978年）的报告相反。对3B1-2染色体畸变的运动活动和羽化表型的分析，没有发现这两种节律在遗传控制上的差异。3B1-2染色体畸变、三个周期素突变等位基因和周期素基因重复的时钟表型表明，周期素基因座的突变分别通过增加、减少或消除周期素活性来缩短、延长或消除周期性。
