Devadhasan Anush, Kolodny Oren, Carja Oana
Computational Biology Department, School of Computer Science, Carnegie Mellon University, Pittsburgh, Pennsylvania, United States of America.
Department of Ecology, Evolution, and Behavior, E. Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel.
PLoS Comput Biol. 2024 Nov 22;20(11):e1012542. doi: 10.1371/journal.pcbi.1012542. eCollection 2024 Nov.
Many evolving ecosystems have spatial structures that can be conceptualized as networks, with nodes representing individuals or homogeneous subpopulations and links the patterns of spread between them. Prior models of evolution on networks do not take ecological niche differences and eco-evolutionary interplay into account. Here, we combine a resource competition model with evolutionary graph theory to study how heterogeneous topological structure shapes evolutionary dynamics under global frequency-dependent ecological interactions. We find that the addition of ecological competition for resources can produce a reversal of roles between amplifier and suppressor networks for deleterious mutants entering the population. We show that this effect is a nonlinear function of ecological niche overlap and discuss intuition for the observed dynamics using simulations and analytical approximations. We use these theoretical results together with spatial representations from imaging data to show that, for ductal carcinoma, where tumor growth is highly spatially constrained, with cells confined to a tree-like network of ducts, the topological structure can lead to higher rates of deleterious mutant hitchhiking with metabolic driver mutations, compared to tumors characterized by different spatial topologies.
许多不断演化的生态系统具有可被概念化为网络的空间结构，其中节点代表个体或同质亚种群，而边代表它们之间的传播模式。先前的网络进化模型没有考虑生态位差异和生态 - 进化相互作用。在这里，我们将资源竞争模型与进化图论相结合，以研究在全球频率依赖性生态相互作用下，异质拓扑结构如何塑造进化动态。我们发现，对资源的生态竞争的加入可以使有害突变体进入种群时，放大器网络和抑制器网络之间的角色发生逆转。我们表明，这种效应是生态位重叠的非线性函数，并使用模拟和解析近似来讨论观察到的动态的直觉。我们将这些理论结果与成像数据的空间表示相结合，以表明，对于导管癌，肿瘤生长在空间上受到高度限制，细胞局限于树状的导管网络，与具有不同空间拓扑结构的肿瘤相比，拓扑结构可导致有害突变体与代谢驱动突变一起搭便车的发生率更高。
