An Integrative Approach to the Evolutionary Assembly of Vertebrate Body Plans

动物形态-在其所有的多样性-代表少至40+身体计划。这些基本模式如何起源仍然是进化生物学的核心追求。然而，一个身体计划的演变需要非递增的过渡，并不容易适合人口水平的过程模型。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前途的模型，该模型表达了作为种群水平波动的主要表型转变。我的长期目标是揭示在早期脊椎动物中限制和促进表型进化的机制。有了这个目标，我调查如何主要离散变化：a）出现; B）成为渠道;和c）增加差距。为了做到这一点，我专注于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-躯干边界（HTB）。我假设主要的表型变异来自：a）反应规范的渠道化;和B）功能链接的增加。这一假说产生了以下预测：1）可塑性介导由新等位基因引起的功能变异，改变连锁性状的反应规范（在OA中测试）; 2）反应规范变得渠道化（OA）; 3）与新性状功能相关的性状进化速率比性状本身增加（OA，CNS，HTB）。OA：我将揭示以前未知的OA剧目在脊椎动物：a）喂养的下巴运动的情况下，观察斑马鱼突变体缺乏下巴关节;和B）新重建的口腔光盘干七鳃鳗，建议一个独特的组装吸盘。我的目标是测试，使用斑马鱼突变体，如何对颌骨破坏（种群水平波动）进行塑料反应，使修改后的吸力喂养，以及这种反应是否具有任何潜在的遗传固定。中枢神经系统：最近的一项发现揭示了非脊索动物外群（半脊索动物）中的脊椎动物样“脑”信号中心。然而，目前尚不清楚在看似简单的半索神经系统中是否存在基因网络或隐藏的复杂性。为了验证这一点，我将绘制半索动物的神经回路。HTB：有颌脊椎动物有一个完整的HTB，但在没有中间形式的情况下，这种转变似乎是跳跃式的。我的目标是确定一个过渡状态的HTB进化的一个姐妹组的有颌脊椎动物。这将限制HTB结构（颈部，心脏，胸鳍）在脊椎动物体内进化的时间和方式。在整个项目中，我调查的机制，发育和功能，产生了脊椎动物的身体计划，也支配我们的解剖。无颌突变斑马鱼为解决一个长期存在的问题提供了一条新途径：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.