The genetic basis for the evolution of altruism during the transition to multicellularity

利他主义——一种对自己付出代价但对他人有益的行为的能力，是从社会行为到个体进化转变的各种生物现象进化的核心。尽管人们对利他主义的选择条件越来越了解，但这种行为的遗传基础的进化起源仍然难以捉摸。利他主义最极端的形式是生殖利他主义和自杀。在多细胞生物中，它们的典型特征是发育过程中不育体细胞的分化和受损或突变细胞的细胞自杀程序的启动。本研究计划的目标是研究在向多细胞过渡过程中生殖利他主义（即体细胞）和细胞自杀（程序性细胞死亡，PCD）进化的遗传基础。我们的一般假设是，利他主义的进化涉及基因的共同选择和调控回路的修改，这些回路涉及对变化/压力环境的反应。在多细胞生物进化过程中，利他主义的进化涉及到环境线索的调节途径的共同选择，这一发现将(i)补充并支持最近提出的观点，即分化和社会进化涉及到与孤立生物感知/处理环境刺激相关的调节回路的重塑；（ii）认为在分子水平上利他主义进化的一般原理是可以确定的。此外，关于PCD进化的信息将有助于我们理解调节PCD和细胞增殖的信号通路，并可以提高我们预测包括人类在内的复杂多细胞生物中这些通路扰动的后果的能力。

Altruism - the capacity to perform acts costly to self but beneficial to others, is central to the evolution of various biological phenomena from social behavior to evolutionary transitions in individuality. Although the selective conditions favoring altruism are being increasingly understood, the evolutionary origins of the genetic basis for this behavior remain elusive. The most extreme forms of altruism are reproductive altruism and suicide. In multicellular organisms, they are typified by the differentiation of sterile somatic cells during development and the launch of the cell suicide program in damaged or mutated cells. The goal of this research program is to investigate the genetic basis for the evolution of reproductive altruism (i.e., soma) and cell suicide (programmed cell death, PCD) during the transition to multicellularity. Our general hypothesis is that the evolution of altruism involved the co-option of genes and modification of regulatory circuits implicated in the response to changing/stressful environments. The finding that the evolution of altruism during the evolution of multicellularity involved the co-option of a regulatory pathway conditioned on environmental cues will (i) complement and provide support to recent proposals that cast differentiation and social evolution involved the remodeling of regulatory circuits associated with the perception/processing of environmental stimuli by solitary organisms, and (ii) argue that general principles underlying the evolution of altruism at the molecular level can be identified. In addition, information on the evolution of PCD will facilitate our understanding of signaling pathways regulating PCD and cell proliferation and can improve our ability to predict the consequences of perturbations in these pathways in complex multicellular organisms, including humans.