Evolution of a developmental gene regulatory network during a life history switch in Heliocidaris

多细胞生物表现出惊人的多样性的生活史策略，包括广泛的寿命，首次繁殖的时间，一生的繁殖力，和母亲的投资。生活史特征通常独立于成体形态而进化，并且对生物体如何相互作用和适应环境具有重要影响。在动物中，一个特别引人注目的生活史变化是胚胎发育加速，这在包括高捕食和有限资源在内的各种条件下都是有利的。一个成熟的理论体系提供了关于生命史中这些变化为什么会进化的见解，但对如何进化的了解要少得多。该项目的中心目标是确定在生命史的实质性转变过程中特定性状变化的遗传和分子基础。该研究系统是一组非常密切相关但在生活史特征方面高度不同的海胆物种，包括生殖力，幼虫形式和早期发育速度的显着差异。该项目使用尖端技术，包括表观遗传学测定，单细胞测序和基因组编辑，以确定有助于一系列生活史特征的基因功能变化。这些研究将为了解生命史和发育机制如何演变提供基本见解。了解分子机制的改变如何促进性状和适应是基础科学，在医学，农业和生物技术中具有重要的应用。生活史性状是生物多样性的主要组成部分，构成了多细胞生物的一套基本适应，但其发育和遗传基础仍然知之甚少，特别是在形态学和生理学方面。该项目旨在确定基因组和发育机制中的变化，这些变化在海胆属Heliocidaris中产生了戏剧性的生活史转变，即从营养型（小卵，高繁殖力，喂养幼虫）和营养型（大卵，低繁殖力，非喂养幼虫）。这个属是非常适合解决的动机问题，因为它包含的物种有显着不同的生活史，尽管非常密切的系统发育关系，因为祖先的发育基因调控网络（GRN）的海胆已被详细描述。该项目的目标是了解早期发育的关键分子机制在进化过程中是如何改变的，以加速卵营养菌的前变质，以及它们是如何做到这一点而不影响其他性状的。这些目标将通过全面表征发育过程中的调控状态来实现，以确定候选调控分子和在卵磷脂营养起源过程中保守或改变的相互作用;（GRN中的节点）了解它们的发育功能，可能的相互作用，以及对卵磷脂营养起源的贡献;以及鉴定和干扰可能介导改变的相互作用的候选基因调控元件（GRN中的边缘）了解它们的分子功能和对卵磷脂营养起源的贡献。该奖项反映了NSF的法定使命，并通过评估被认为值得支持使用基金会的知识价值和更广泛的影响审查标准。

Multicellular organisms exhibit an astonishing diversity of life history strategies, including a wide range of lifespan, time to first reproduction, lifetime fecundity, and maternal investment. Life history traits often evolve independently of adult morphology and are a major influence on how organisms interact with each other and adapt to their environment. A particularly striking life history change in animals is accelerated embryonic development, which is favored under a variety of conditions including high predation and limited resources. A mature body of theory provides insights into why such changes in life histories evolve, but far less is known about how. The central objective of this project is to identify the genetic and molecular basis for changes in specific traits during a substantive shift in life history. The study system is a group of sea urchin species that are very closely related yet highly divergent in terms of life history traits, including striking differences in fecundity, larval form, and rate of early development. This project uses cutting-edge technologies, including epigenetic assays, single-cell sequencing, and genome editing to identify changes in gene function that contributed to a suite of life history traits. These studies will provide basic insights into how life histories and developmental mechanisms evolve. Understanding how alterations in molecular mechanisms contribute to traits and to adaptation is fundamental science that has important applications in medicine, agriculture, and biotechnology.Life history traits are a major component of biological diversity and constitute a fundamental set of adaptations in multicellular organisms, but their developmental and genetic basis remains poorly understood, particularly in relation to morphology and physiology. This project seeks to identify changes in the genome and in developmental mechanisms that produced a dramatic life history transformation within the sea urchin genus Heliocidaris, namely from planktotrophy (small eggs, high fecundity, feeding larvae) and lecithotrophy (large eggs, low fecundity, nonfeeding larvae). This genus is well suited to addressing the motivating questions because it contains species with dramatically divergent life histories despite very close phylogenetic relationships, and because the ancestral developmental gene regulatory network (GRN) of sea urchins has been characterized in detail. The goals of the project are to learn how critical molecular mechanisms of early development were altered during the course of evolution so as to accelerate premetamorphic the lecithotroph, and how they did so without perturbing other traits. These goals will be achieved by comprehensively characterizing regulatory states during development to identify candidate regulatory molecules and interactions that have been conserved or altered during the origin of lecithotrophy; experimentally perturbing candidate proteins (nodes in the GRN) to learn about their developmental function, likely interactors, and contributions to the origin of lecithotrophy; and identifying and perturbing candidate gene regulatory elements that may mediate altered interactions (edges in the GRN) to understand their molecular function and contributions to the origin of lecithotrophy.This award reflects NSF's statutory mission and has been deemed worthy of support through evaluation using the Foundation's intellectual merit and broader impacts review criteria.