Collaborative Research: The Proximate Basis of Individual Variation in Phenotypic Plasticity

在所有动物中，生长过程中食物获取的变化会影响最终成年体型。更多的营养会产生更大的成年人。 然而，生物体的所有部分并非以相同的速度生长，因此生长过程中营养获取的变化会对身体不同部分的最终大小产生不同的影响。 尽管营养变化对相对性状大小的影响已有充分记录，但直到最近才有工具可以用于（i）研究遗传和发育机制如何管理性状的生长以产生适当比例的成年体，以及（ii）研究这些机制如何改变以改变生长模式以产生物种之间的大小多样性。 在这里，研究人员将采取一种新颖的方法，通过改变果蝇品系的饮食，每个果蝇品系都拥有自己独特且已知的遗传密码，以确定身体各部分生长调节和整合背后的特定基因。 这项研究将与一项新的、有趣的小学计算机学习活动相结合，学生将改变虚拟生物结构的相对生长，将年轻人转变为梦幻般的生物。表型可塑性是基因型在环境中表达不同表型的能力。 它在现象学层面上得到了充分的研究，特别是形态特征；表型可塑性可以阻碍或促进适应，导致进化新奇的发生或作为适应本身。 由于缺乏实验工具，这意味着形态可塑性进化的两个核心组成部分——个体之间可塑性反应表达的变异以及这种变异的近似基础——基本上是未知的。 营养引起的体型变化对于所有后生动物来说都是常见的：个体发育过程中的营养限制通常会产生比营养丰富的饮食更小的个体，尽管营养引起的体型可塑性程度在形态特征之间可能存在巨大差异。 相对性状可塑性的这种差异植根于最近发现的发育遗传机制，该机制调节和整合性状的生长以响应营养变化。 Frankino (PI) 和 Shingleton (co-PI) 假设这些相同机制的变异是性状可塑性基因型之间进化上重要变异的基础。在这里，他们建议通过以下方式检验这一假设：（i）应用新方法来创建和量化营养引起的性状和体型可塑性的个体差异； (ii) 使用全基因组关联作图来识别导致这种变异的基因，以及； (iii)采用一系列发育测定来确认这些基因在营养诱导的体型可塑性的个体差异中的作用。

In all animals, changes in access to food during growth affects final adult size; greater nutrition produces larger adults. However, not all parts of an organism grow at the same rate, and so changes in access to nutrition during growth can affect the ultimate size of different parts of the body differently. Although the effects of nutritional variation on relative trait size are well documented, only recently have the tools become available to (i) enable study of how genetic and developmental mechanisms manage the growth of traits to produce a properly proportioned adult and to (ii) enable study of how these mechanisms change to alter growth patterns to produce size diversity among species. Here, the investigators will take a novel approach by changing diet in lines of fruit flies, each possessing their own unique and known genetic code, to identify the specific genes underlying the regulation and integration of growth among various parts of the body. This research will be coupled with a new, fun elementary school computer-based learning activity where students will alter the relative growth of structures in virtual creatures, transforming young humans into fantastical beings.Phenotypic plasticity is the ability of a genotype to express different phenotypes across environments. It is well studied on a phenomenological level, particularly for morphological traits; phenotypic plasticity can hinder or promote adaptation, lead to the genesis of evolutionary novelties or serve as an adaptation itself. A lack of experimental tools has meant that two components central to the evolution of morphological plasticity - the variation among individuals in the expression of plastic responses and the proximate bases of this variation - are essentially unknown. Nutritionally-induced size variation is common to all metazoans: nutritional limitation during ontogeny generally produces smaller individuals than does a nutritionally rich diet, although the degree of nutritionally-induced size plasticity can vary dramatically among morphological traits. Such differences in relative trait plasticity are rooted in recently identified developmental genetic mechanisms that regulate and integrate the growth of traits in response to nutritional variation. Frankino (PI) and Shingleton (co-PI) hypothesize that variation in these same mechanisms underlies the evolutionarily important variation among genotypes in trait plasticity. Here, they propose to test this hypothesis by: (i) applying new methods to create and quantify the among-individual variation in nutritionally-induced trait and body size plasticities; (ii) using genome-wide association mapping to identify genes that contribute to this variation, and; (iii) employing a series of developmental assays to confirm the role of these genes in producing among-individual variation in nutritionally induced size plasticity.