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

表型可塑性对快速进化适应的作用：使用赤拟谷盗和苏云金芽孢杆菌的理论和实验方法。

• 批准号: 274553442
• 负责人: Professor Dr. Joachim Kurtz
• 金额: --
• 依托单位: Institut für Klinische Molekularbiologie
• 依托单位国家: 德国
• 项目类别: Priority Programmes
• 财政年份: 2015
• 资助国家: 德国
• 起止时间: 2014-12-31 至 2021-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/274553442?language=en
• 关键词: role; phenotypic; plasticity; rapid; evolutionary

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.

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因素。拟议的项目旨在通过研究表型可塑性的一个主要例子来阐明快速适应的条件，无脊椎动物免疫记忆(即。“启动”)。利用实验进化、群体遗传学和数学建模的结合，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（这里是免疫启动）是否也会选择毒性更强的病原体。我们将通过对苏云金芽孢杆菌（Bacillus thuringiensis）在表型塑料与非塑料（即引物与非引物）castaneum宿主中的连续传代实验来解决这个问题，并通过额外的数学建模来解释实证结果。(2)寄主表型可塑性对寄主自身的快速适应有何影响？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）变化。我们将通过一系列实验来解决这个问题，这些实验主要关注宿主在有和没有实验诱导的可塑性的情况下的进化（这里是免疫启动）。(3)在哪些条件下，表型可塑性导致快速遗传同化？人们常说，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存在的环境与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，进行一系列交替处理的实验，模拟不同类型的环境波动。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，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。