The genomic basis for adaptation to a fungal pathogen

项目摘要 本项目将确定对Beauvaria的进化抗性的基因组基础 在遗传模式昆虫黑腹果蝇中，昆虫病原真菌，如 作为B。球孢白僵菌，用于登革热和疟疾的蚊子媒介的生物控制， 以及其他害虫，如臭虫和影响粮食安全的害虫。然而，在这方面， 昆虫对真菌昆虫病原体的抗性机制知之甚少。 了解耐药性对人类健康有额外的影响，因为耐药性的强 昆虫和哺乳动物先天免疫系统之间的同源性。一个“进化和重新排序” 方法将被应用于确定进化的抗真菌感染的遗传基础 在果蝇中。D.将人工选择黑腹果蝇以增加对B的抗性。 bassiana在非常大的，复制实验种群。预选来源人群 将来自D.黑腹菌代表常见的自然 世界各地的变化。全基因组序列数据将从选定的和对照的样本中收集。 种群在多个中间世代在整个选择制度，允许 观察适应性等位基因的时间轨迹。预计， 选择将主要来自常设的遗传变异，所以这些等位基因频率 动力学将说明在自然界中人们所知甚少的“软扫描”适应模式， 人口。这项研究将确定形成抗真菌防御的机制因素， 包括阐明抗性中显著的两性异形的基础，并将有助于 作为适应性进化的一般模型。

Project Summary The present project will determine the genomic basis for evolved resistance to Beauvaria bassiana in the genetic model insect, Drosophila melanogaster. Entomopathogenic fungi, such as B. bassiana, are used in biological control of mosquito vectors of dengue fever and malaria, and of other insect pests, such as bedbugs and those that affect food security. However, mechanisms of insect resistance to fungal entomopathogens are poorly understood. Understanding resistance has additional implications for human health because of strong homology between insect and mammalian innate immune systems. An "evolve and resequence" approach will be applied to determine the genetic basis for evolved resistance to fungal infection in Drosophila. D. melanogaster will be artificially selected for increased resistance to B. bassiana in very large, replicated experimental populations. The pre-selection source population will be derived from a cosmopolitan sample of D. melanogaster representing common natural variation worldwide. Whole-genome sequence data will be collected from selected and control populations at multiple intermediate generations throughout the selection regime, allowing observation of the temporal trajectory of adaptive alleles. It is expected that the response to selection will primarily derive from standing genetic variation, so these allele frequency dynamics will illustrate the poorly understood "soft sweep" mode of adaptation in natural populations. This study will determine mechanistic factors that shape antifungal defense, including elucidation of the basis for a striking sexual dimorphism in resistance, and will serve as a general model of adaptive evolution.