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的成年体型;更多的营养会产生更大的成年体。 然而，并非生物体的所有部分都以相同的速度生长，因此生长过程中营养获取的变化可能会对身体不同部位的最终大小产生不同的影响。 虽然营养变化对相对性状大小的影响有据可查，但直到最近才有工具可用于（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人，以及（ii）研究这些机制如何改变生长模式以产生物种间的大小多样性。 在这里，研究人员将采取一种新的方法，通过改变果蝇的饮食，每个果蝇都拥有自己独特的和已知的遗传密码，以确定调节和整合身体各部分生长的特定基因。 这项研究将结合一个新的，有趣的小学计算机为基础的学习活动，学生将改变虚拟生物的结构的相对增长，把年轻人变成幻想的生物。表型可塑性是基因型在不同环境中表达不同表型的能力。 它在现象学水平上得到了很好的研究，特别是在形态特征方面;表型可塑性可以阻碍或促进适应，导致进化新奇性的发生或作为适应本身。 缺乏实验工具意味着形态可塑性进化的两个核心组成部分--个体间可塑性反应表达的变异和这种变异的基本基础--基本上是未知的。 营养诱导的大小变化是常见的所有后生动物：在个体发育过程中的营养限制通常产生较小的个体比营养丰富的饮食，虽然营养诱导的大小可塑性的程度可以显着不同的形态特征。 这种相对性状可塑性的差异植根于最近确定的发育遗传机制，调节和整合响应营养变化的性状的生长。 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间进化上重要变异的基础。在这里，他们建议通过以下方法来测试这一假设：（i）应用新方法来创建和量化营养诱导的性状和体型可塑性的个体差异;（ii）使用全基因组关联映射来识别导致这种变异的基因;以及（iii）采用一系列的发育试验，以确定这些基因在产生以下基因中的作用-个体差异在营养诱导的大小可塑性。

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.