GENETICS OF INSECTICIDE RESISTANCE IN DROSOPHILA

昆虫种群对杀虫压力的可预测反应是 抗药性的发展。尽管负责的生理机制 因为昆虫对杀虫剂的抗药性是相当清楚的， 对导致基因变化的基因变化知之甚少 抵抗。这项拟议的研究将调查基因的光谱。 果蝇可能发生的变化，以增强对 对两种化合物中的任何一种进行致命的应用。所选择的化合物 是保幼激素III，一种自然产生的昆虫激素，以及 甲基丁二烯，一种在化学和生物上模拟的杀虫剂 保幼激素；两者在纳米克剂量下对果蝇都是致命的 级别。导致抗药性的几种类型的基因变化将是 检查过了。点突变株将用诱变剂诱变，而抗病突变株 任何一种化合物的毒性水平都将被选择。负责的地点 将被描述并绘制成地图。在平行实验中，两只果蝇 人口将受到这两种药物中任何一种的亚致死剂量 化合物，以便筛选出30-50代的抗性菌株。 一个种群将是等基因的易感野生型菌株，另一个种群将是等基因敏感的野生型菌株。 将是一个品系间杂交，将导致杂交不育 后代种群。导致抗性的基因座将是 特征，图谱，并与来自突变的那些进行比较 屏幕上。最后，阻力机制(穿透力的变化， 新陈代谢或有毒化合物的排泄)将在 应用放射性标记的每个基因座的代表性突变 保幼激素III或甲基丁二烯。这项工作的结果将是 对于理解类型(点状、自发、异常)很重要， 基因组位置和突变的相对频率 抗药性的发展。

A predictable response of an insect population to insedticidal pressure is resistance development. Although the physiological mechanisms responsible for insect resistance to insecticides are fairly well understood, relatively little is known about the genetic changes which bring about resistance. The proposed research will investigate the spectrum of genetic changes which can occur in Drosophila melanogaster to confer resistance to lethal application does of either of two compounds. The compounds chosen are juvenile hormone III, a naturally occurring insect hormone, and methoprene, an insecticide which chemically and biologically mimics juvenile hormone; both are lethal to Drosophila when applied in nanogram levels. Several types of genetic changes resulting in resistance will be examined. Point mutants will be induced with a mutagen and those resistant to toxic levels of either compound will be selected. The responsible loci will be characterized and mapped. In parrallel experiments, two Drosophila populations will be subjected to sublethal doses of either of these compounds in order to select for resistant strains for 30-50 generations. One population will be isogenic susceptible wild-type strain, and the other will be an interstrain cross which will result in hybrid dysgenesis in progeny populations. Loci responsible for resistance will be characterized, mapped, and compared to those derived from the mutagenesis screen. Finally, the mechanism of resistance (changes in penetration, metabolism, or excretion of the toxic compound) will be determined in a representative mutant of each locus by application of radiolabelled juvenile hormone III or methoprene. The results of this work will be important for understanding the types (point, spontaneous, dysgenic), genomic location, and relative frequency of mutations responsible for resistance development.