Mechanisms and Costs of Adaptive Plasticity in a Starlet Anemone (Nematostella Vectensis) Model

星海葵（Nematostella Vectensis）模型中自适应可塑性的机制和成本

• 批准号: RGPIN-2021-03142
• 负责人: Little, Alexander
• 金额: $ 0.2万
• 依托单位: Queen's University
• 依托单位国家: 加拿大
• 项目类别: Discovery Grants Program - Individual
• 财政年份: 2022
• 资助国家: 加拿大
• 起止时间: 2022-01-01 至 2023-12-31
• 项目状态: 已结题
• 来源: https://www.nserc-crsng.gc.ca/ase-oro/Details-Detailles_eng.asp?id=745785
• 关键词: Mechanisms; Costs; Adaptive; Plasticity; Starlet

Adaptive plasticity arguably represents the best defense animals have against the mounting effects of climate change. However, stressor interactions can undermine this important defense. My research uses a bottom-up approach to identify the signaling pathways that regulate plastic responses to environmental stress in a starlet anemone (Nematostella vectensis) model. The proposed work also capitalizes on the clonal ability of N. vectensis to test whether plasticity carries inherent costs. My first objective seeks to identify the molecular pathways that regulate plastic responses to thermal, osmotic, hypoxic, and nutritional stress. Nuclear receptors (NRs) represent strong candidates to integrate environmental inputs with cellular responses because they function both as small molecule receptors and regulators of large-scale transcriptional networks. My lab will investigate three N. vectensis NRs: i) an ortholog of vertebrate hepatocyte nuclear factor 4a, ii) a cnidarian-specific retinoid X receptor subfamily member, and iii) a Tailles subfamily member. Importantly, these three NRs have been associated with plastic responses in a number of animal systems. Using custom transgenic lines for each of these NRs, my lab will test how their expression levels, DNA-binding dynamics, protein-interaction networks, and activity patterns respond to shifts in temperature, salinity, oxygenation, and nutrient availability. This objective co-opts my expertise in high-throughput drug screening - but to screen for environmental stressors instead. My second objective will use overlaps in signalling pathways (identified in objective 1) to predict stressor interactions that manifest ecological costs of plasticity. For example, if a given NR regulates responses to both thermal and osmotic stress, we would expect that certain temperature-salinity combinations could undermine plasticity. Thermal stress, for instance, might a) jam the signaling pathways that coordinate responses to osmotic stress, or b) induce a phenotype that has increased vulnerability to osmotic stress. By quantifying the capacity for plasticity in wild-collected genotypes and measuring physiological performance traits (i.e., metabolic rate, developmental rate, growth rate), my lab can test whether specific stressor interactions promote ecological costs. If there are ecological costs associated with plasticity, we would expect performance traits to be most disrupted in genotypes with the highest capacities for plasticity. Collectively, this program will help provide a predictive framework to model the ecological costs of plasticity - a goal that is increasingly critical with the effects of climate change. In addition to providing a more comprehensive understanding of NR signalling and evolution, this work will help identify novel barriers to climate change responses and help determine whether plasticity will be enough to overcome the increasingly complex and rapid changes in environment animals face.

适应性可塑性可以说是动物对气候变化影响的最佳防御。然而，压力源的相互作用可能会破坏这一重要的防御。我的研究使用自下而上的方法来确定调节塑料对环境压力的反应的信号通路在一个星海葵（Nematostella vectensis）模型。这项工作还利用了N. vectens测试是否可塑性进行固有成本。我的第一个目标是确定调节塑料对热，渗透压，缺氧和营养应激反应的分子途径。核受体（NR）代表了整合环境输入与细胞反应的强有力的候选者，因为它们既作为小分子受体又作为大规模转录网络的调节因子。我的实验室将研究三个N。vectensis NR：i）脊椎动物肝细胞核因子4a的直系同源物，ii）刺胞动物特异性类视黄醇X受体亚家族成员，和iii）Tailles亚家族成员。重要的是，这三种NR与许多动物系统中的塑料反应有关。使用这些NR的定制转基因品系，我的实验室将测试它们的表达水平，DNA结合动力学，蛋白质相互作用网络和活动模式如何响应温度，盐度，氧合和营养物质可用性的变化。这一目标利用了我在高通量药物筛选方面的专业知识，但要筛选环境压力因素。我的第二个目标将使用信号通路的重叠（目标1中确定）来预测表现可塑性生态成本的压力源相互作用。例如，如果一个给定的NR调节对热胁迫和渗透胁迫的反应，我们预计某些温度-盐度组合可能会破坏可塑性。例如，热应激可能a）堵塞协调对渗透应激的反应的信号通路，或B）诱导对渗透应激具有增加的脆弱性的表型。通过量化野生收集的基因型的可塑性能力和测量生理性能性状（即，代谢率，发育率，生长率），我的实验室可以测试特定的压力相互作用是否会促进生态成本。如果存在与可塑性相关的生态成本，我们可以预期，具有最高可塑性能力的基因型的性能性状受到的破坏最大。总的来说，该计划将有助于提供一个预测框架，以模拟可塑性的生态成本-这一目标对气候变化的影响越来越重要。除了提供对NR信号传导和进化的更全面的理解外，这项工作还将有助于确定气候变化响应的新障碍，并有助于确定可塑性是否足以克服动物面临的日益复杂和快速的环境变化。