A Study of the Genetic Determinants of a Model Host-Parasite System

本研究的目的是阐明昆虫宿主抗寄生的机制和遗传基础。先前的生态学研究表明，这种寄生虫（一种大螯螨）会损害其宿主（一种果蝇）的多种生殖特征，这为提出寄生在这种自然系统中进化潜力的具体问题提供了理论依据。利用遗传上不同的抗性和控制系以及综合的行为和生理技术，提出了实验室实验，以确定(1)自然宿主种群中抗性的遗传变异性的大小，(2)抗性进化的限制，(3)遗传变异性的丧失（通过控制宿主近亲繁殖）对寄生率的影响，以及(4)赋予抗性的宿主性状。关于抵抗寄生虫和病原体的遗传变异模式及其对自然界疾病分布的影响，我们所知道的大部分知识来自对植物及其天敌的研究。只有在动物宿主中获得必要的信息，我们才能开始发展寄生虫耐药性进化的一般理论，以及疾病控制的合理方法。提出的研究旨在利用生态学众所周知的昆虫-体外寄生虫模型实现这一目标。这些结果应该具有广泛的意义，因为体外寄生虫无处不在，是许多物种中已知的媒介或传染性寄生虫病，并且因为目前系统中介导体外寄生虫易感性的机制与其他分类群（包括鸟类、哺乳动物和其他无脊椎动物）的机制有很强的相似性。

Polak 9726903 The goals of the proposed work are to elucidate the mechanistic and genetic bases of resistance against parasitism in an insect host. Previous ecological research has shown that the parasite (a macrochelid mite) damages multiple reproductive traits of its host (a drosophilid fly), providing the rationale for asking specific questions about the evolutionary potential of parasitism in this natural system. Laboratory experiments, using genetically distinct resistant and control lines of flies and integrated behavioral and physiological techniques, are proposed to determine (1) the magnitude of genetic variability underlying resistance in the natural host population, (2) constraints on the evolution of resistance, (3) effects of loss of genetic variability (through controlled host inbreeding) on rates of parasitism, and (4) traits of the host that confer resistance. Most of what is known about patterns of genetic variability in resistance against parasites and pathogens, and their effect on the distribution of disease in nature, comes from studies of plants and their natural enemies. Only by acquiring the requisite information in animal hosts can we begin to develop a general theory of the evolution of parasite resistance, and sound approaches to disease control. The proposed study is aimed at attaining this goal using an insect-ectoparasite model whose ecology is well known. The results should have broad-ranging implications because ectoparasites are ubiquitous, are know vectors or transmissible parasitic disease in numerous species, and because the mechanisms expected to mediate susceptibility to ectoparasitism in the present system have strong parallels with that in other taxa including birds, mammals and other invertebrates.