The role of phenotypic plasticity for rapid evolutionary adaptation: theoretical and experimental approaches using Tribolium castaneum and Bacillus thuringiensis.

表型可塑性和寄主-寄生虫的相互作用被认为是快速进化过程的主要驱动因素。这项拟议的项目旨在通过研究表型可塑性的一个主要例子--无脊椎动物的免疫记忆(即启动)来阐明快速适应的条件。利用实验进化、种群遗传学和数学建模的组合，我们建议研究以下三个问题。(1)寄主表型可塑性对病原体快速适应的影响是什么？我们的初步理论工作表明，抗性寄主选择毒力强的病原菌。这就提出了一个问题，表型塑料宿主(这里：免疫启动)是否也会选择更致命的病原体。我们将通过昆虫病原苏云金芽孢杆菌在典型塑料和非塑料(即引种和非引种)赤霉菌宿主中的一系列传代实验来解决这个问题，并建立额外的数学模型来解释经验结果。(2)寄主的表型可塑性对寄主自身的快速适应有何影响？通常认为，高度的表型可塑性限制了进化适应，因为它可能缓冲遗传(即进化)变化。我们将通过一系列实验来解决这个问题，这些实验侧重于在有和没有实验诱导可塑性(这里：免疫启动)的情况下的宿主进化。(3)在什么条件下，表型可塑性导致快速遗传同化？人们经常说，波动的环境有利于表型可塑性，并阻止遗传同化的进化。然而，这些论点往往忽略了诱导塑料表型时存在的环境和实际发生表型选择的环境之间的差异。“免疫启动”的美妙之处在于，它允许在进化实验中将这两种环境分开。我们将充分利用这一功能，进行一系列实验，模拟不同类型的环境波动进行交替治疗。研究问题(2)和(3)的实验结果将用群体遗传学模型描述。这将作为一个起点，为表型可塑性在遗传分化和物种形成中的作用发展一个一般的理论框架。

Phenotypic plasticity and host-parasite interactions are thought to be major drivers of fast evolutionary processes. The proposed project aims at elucidating conditions for rapid adaptation by investigating a prime example of phenotypic plasticity, the invertebrate immune memory (i.e. 'priming'). Using a combination of experimental evolution, population genetics, and mathematical modeling, we propose to investigate the following three questions. (1) What is the effect of host phenotypic plasticity on rapid adaptation of a pathogen? Our preliminary theoretical work showed that resistant hosts select for virulent pathogens. This raises the question whether phenotypically plastic hosts (here: with immune priming) might select for more virulent pathogens, too. We will address this topic with a serial passage experiment of the entomopathogen Bacillus thuringiensis in phenotypically plastic vs. non-plastic (i.e. primed vs. non-primed) Tribolium castaneum hosts, and additional mathematical modeling in order to explain the empirical results. (2) What is the effect of host phenotypic plasticity on rapid adaptation of the host itself? It is generally assumed that a high degree of phenotypic plasticity constrains evolutionary adaptation, since it may buffer genetic (i.e. evolutionary) changes. We will address this topic with a series of experiments that focus on host evolution with and without experimentally induced plasticity (here: immune priming). (3) Under which conditions does phenotypic plasticity result in rapid genetic assimilation? It is often stated that fluctuating environments favor phenotypic plasticity and prevent the evolution of genetic assimilation. However, these arguments tend to overlook the difference between the environment that is present when plastic phenotypes are induced, and the environment, in which selection of the phenotypes actually happens. The beauty of 'immune priming' is that it allows disentangling these two environments in evolutionary experiments. We will make full use of this feature and conduct a series of experiments with alternating treatments that mimic different types of environmental fluctuations. The experimental results of research questions (2) and (3) will be described with a population genetics model. This will serve as a starting point to develop a general theoretical framework for the role of phenotypic plasticity on genetic divergence and speciation.