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

表型可塑性和宿主-寄生虫相互作用被认为是快速进化过程的主要驱动力。拟议的项目旨在通过研究表型可塑性的一个主要例子，即无脊椎动物的免疫记忆（即“引发”），阐明快速适应的条件。使用实验进化，群体遗传学和数学建模的组合，我们建议调查以下三个问题。(1)寄主表型可塑性对病原体的快速适应有什么影响？我们的初步理论工作表明，抗性宿主选择毒性病原体。这就提出了一个问题，即表型可塑性宿主（这里：有免疫启动）是否也可能选择毒性更强的病原体。我们将解决这个问题的昆虫病原体苏云金芽孢杆菌在表型塑料与非塑料（即引发与非引发）赤拟谷盗宿主的连续传代实验，以及额外的数学建模，以解释实证结果。(2)宿主表型可塑性对宿主自身的快速适应有什么影响？一般认为，高度的表型可塑性限制了进化适应，因为它可以缓冲遗传（即进化）的变化。我们将通过一系列实验来解决这个问题，这些实验专注于有和没有实验诱导可塑性的宿主进化（在这里：免疫启动）。(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可塑性表型时所存在的环境与表型选择实际发生的环境之间的差异。“免疫启动”的美妙之处在于，它允许在进化实验中解开这两种环境的纠缠。我们将充分利用这一特点，进行一系列模拟不同类型环境波动的交替处理实验。研究问题（2）和（3）的实验结果将用群体遗传学模型来描述。这将作为一个起点，发展一个一般的理论框架的作用，遗传分化和物种形成的表型可塑性。

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.