Evolution and ecology of parasitism and symbiosis in insects

共生是塑造地球上生命的最重要的力量之一。生物学最近的一个重大发展是认识到所有多细胞生物都含有共生微生物。长期以来，这些都是非常难以研究的；然而，分子生物学和计算生物学的进步已经彻底改变了我们对微生物共生的理解。例如，我们刚刚开始理清生活在人类肠道中的数万亿微生物的功能，以及它们在新陈代谢、免疫和发育中的重要作用。事实上，有人认为，如果不包括微生物群，就不能考虑生物体的生态和进化，将生物体视为“全基因组”（即宿主的核、细胞器和共生体基因组的组合）。

Symbiosis is one of the most important forces shaping life on our planet. A major recent development in biology is the realization that all multicellular organisms harbour symbiotic microbes. These have long been incredibly difficult to study; however, advances in molecular and computational biology have revolutionized our understanding of microbial symbiosis. For example, we are just beginning to disentangle the function of the trillions of microbes that live in the human gut, and their important roles in metabolism, immunity, and development. Indeed, it has been argued that one cannot consider the ecology and evolution of an organism without including its microbiota, viewing the organism as a ‘hologenome’ (i.e. the host’s nuclear, organellar, and symbiont genomes combined). My research aims to understand the ecological and evolutionary consequences of symbiosis in insects. Virtually all insects are infected with inherited bacterial symbionts that are transmitted from mothers to their offspring, often in the egg cytoplasm, similar to mitochondria (themselves the descendants of an ancient symbiosis). In maternal transmission, host and symbiont fitness are tightly linked. Indeed, many insect inherited symbionts have evolved to increase the fitness of their hosts, for example by defending them against natural enemies. However, some inherited symbionts manipulate host reproduction to increase the frequency of females, for example by transforming male hosts into females that can then transmit more symbionts. These symbionts, termed ‘reproductive parasites’, highlight the potential for conflicts between symbionts and hosts over transmission. A major aim of this proposal is to examine the consequences of this conflict, for example by asking whether inherited symbionts show reduced function in male hosts (since males are an evolutionary dead end). Tighter still is the link between inherited symbionts and mitochondria, and another major aim of this proposal is to understand how symbionts and mitochondria interact and affect one another, and whether there is co-adaptation between them. Finally, I will examine the effect that other selfish genetic elements that distort sex ratios have on symbionts and mitochondria. I propose to study two insect model systems. The first, the mushroom-feeding fly Drosophila neotestacea, harbours a Spiroplasma bacterial symbiont that protects it against a virulent parasitic nematode. Due to this strong protective benefit, Spiroplasma is spreading rapidly across N. America. The second, the booklouse Liposcelis bostrychophila (a relative of parasitic lice), is polymorphic for an extraordinary maternally inherited sex-ratio distortion, with most females producing only daughters. Also, the mitochondrial genomes of distorting females are ~30% divergent and have a completely different gene order and genome structure than their ‘normal’ counterparts.