An Integrative Approach to the Evolutionary Assembly of Vertebrate Body Plans

动物的形态--尽管种类繁多--只代表了40多个身体形态。这些基本模式是如何起源的，仍然是进化生物学的核心追求。然而，机构计划的演变需要非渐进的过渡，并不容易适应人口一级进程的模型。为了填补这一空白，我最近的工作记录了早期脊椎动物(原始鱼类)的这些转变，并在斑马鱼中产生了一个有希望的模型，该模型将主要表型转变表达为种群水平的波动。我的长期目标是揭示制约和促进早期脊椎动物表型进化的机制。带着这个目标，我调查了主要的离散变异是如何产生的：a)产生；b)变得经典化；以及c)差距扩大。为此，我将重点介绍脊椎动物身体计划的关键组成部分：口腔器官(OA)、中枢神经系统(CNS)和头部-躯干边界(HTB)。我推测，主要的表型变异来自：a)反应规范的通道化；b)功能联系的增加。这一假设产生了如下预测：1)可塑性调节由一个新的等位基因引起的功能变异，即相关性状反应规范的变化(在OA中测试)；2)反应规范变得通道化(OA)；以及3)那些与新性状功能相关的性状进化速度比特征本身更快(OA，CNS，HTB)。OA：我将揭示以前未知的脊椎动物的OA谱系：a)在没有下颌运动的情况下进食，在缺乏颌关节的斑马鱼突变体中观察到；以及b)新重建的七鳃鳗口盘，这表明有一个独特的组装的吸盘。我的目标是使用斑马鱼突变体来测试对颌骨破坏(种群水平波动)的塑料反应如何使修改的吸食成为可能，以及这种反应是否具有任何遗传修复的可能性。中枢神经系统：最近的一项发现发现，在非脊索类外群(半角类)中，存在类似脊椎动物的“脑”信号中心。然而，在看似简单的半中枢神经系统中，是否存在先于结构的基因网络或隐藏的复杂性尚不清楚。为了测试这一点，我将绘制半角形的神经回路图。颌类脊椎动物有一个完整的HTB，但在没有中间形式的情况下，这种转变看起来是跳跃的。我的目标是在颌骨脊椎动物的姐妹群中识别HTB进化的过渡状态。这将限制HTB结构(颈部、心脏、胸鳍)何时以及如何在脊椎动物体内进化。在整个项目中，我研究了产生脊椎动物身体计划并管理我们的解剖学的发育和功能机制。没有下巴的突变斑马鱼为解决一个长期存在的问题提供了一条新的途径：主要变异是如何产生的？这有助于下一阶段：我们的多方面分析，以揭示早期脊椎动物的趋同功能进化或过渡状态。

Animal forms - in all their diversity - represent as few as 40+ body plans. How these basic patterns originated remains a core pursuit of evolutionary biology. However, the evolution of a body plan requires non-incremental transitions and does not readily fit models of population-level processes. To fill in this gap, my recent work has documented these transitions in early vertebrates (primitive fishes) and has also yielded a promising model in zebrafish that express a major phenotypic shift as population-level fluctuations. My long-term objective is to uncover mechanisms that both constrained and facilitated phenotypic evolution in early vertebrates. With that goal, I investigate how major discrete variations: a) arise; b) become canalized; and c) increase in disparity. To do this, I focus on key components of the vertebrate body plan: oral apparatus (OA), central nervous system (CNS), and head-trunk boundary (HTB). I hypothesize that major phenotypic variation emerges from: a) canalization of reaction norms; and b) increase in functional linkages. This hypothesis generates the following predictions: 1)Plasticity mediates functional variation caused by a novel allele, shifting reaction norms of linked traits (tested in OA); 2)Reaction norms become canalized (OA); and 3)Rates of trait evolution increase in those functionally linked to the novel trait more than in the trait itself (OA, CNS, HTB). OA: I will reveal previously unknown OA repertoire in vertebrates: a) feeding in the absence of jaw movement, observed in zebrafish mutants lacking jaw joints; and b) newly reconstructed oral discs of stem lampreys that suggest a uniquely assembled suction cup. I aim to test, using the zebrafish mutants, how plastic responses to the jaw disruption (population-level fluctuations) enabled modified suction feeding, and whether this response harbors any potential to become genetically fixed. CNS: A recent discovery revealed vertebrate-like `brain' signaling centers in non-chordate outgroup (hemichordates). However, it remains unclear whether a gene network preceded structure or hidden complexity exists in the seemingly simple hemichordate nervous system. To test this, I will map neural circuitry in hemichordates. HTB: Jawed vertebrates have a complete HTB, but this transition appears saltatory in the absence of intermediate forms. I aim to identify a transitional state of HTB evolution in a sister group of jawed vertebrates. This will constrain when and how HTB structures (neck, heart, pectoral fins) evolved in a vertebrate body. Throughout this project I investigate the mechanisms, both developmental and functional, that yielded the vertebrate body plan and also govern our anatomy. The jawless mutant zebrafish offer a new path to address a long-standing question: How do major variations arise? This facilitates the next phase: our multifaceted analysis to reveal convergent functional evolution or transitional states in early vertebrates.