GENETICS OF INSECTICIDE RESISTANCE IN DROSOPHILA

昆虫种群对杀虫压力的可预测反应是 抗性发展 虽然生理机制负责 对于昆虫对杀虫剂的抗性是相当好理解的， 相对而言，我们对基因的变化知之甚少， 阻力 拟议的研究将调查遗传谱 黑腹果蝇中可能发生的变化， 两种化合物中的任何一种都是致命的 选择的化合物 是保幼激素III，一种天然存在的昆虫激素， 甲氧普烯，一种化学和生物学上模拟 保幼激素;当以毫微克施用时，这两种激素对果蝇都是致命的 程度. 几种类型的遗传变化导致的阻力将是 考察 点突变体将用诱变剂诱导， 将选择任一化合物的毒性水平。 责任基因座 将被描述和绘制。 在parrandomly实验中，两个果蝇 人口将受到亚致死剂量的这两种 化合物，以选择抗性菌株30-50代。 一个群体将是等基因易感野生型菌株，另一个群体将是等基因易感野生型菌株。 将是一个品系间杂交，这将导致杂种发育不全， 后代种群 负责抵抗的位点将是 表征、作图并与来自诱变的那些进行比较 屏幕 最后，阻力机制（渗透率的变化， 毒性化合物的代谢或排泄）将在 每个基因座的代表性突变体通过应用放射性标记的 保幼激素III或甲氧普烯。 这项工作的结果将是 对于理解类型（点，自发，dysgenic）很重要， 基因组位置，以及负责 抗性发展

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.