Social norms can promote cooperation by assigning reputations to individuals based on their past actions. A good reputation indicates that an individual is likely to reciprocate. A large body of research has established norms of moral assessment that promote cooperation, assuming reputations are objective. But without a centralized institution to provide objective evaluation, opinions about an individual's reputation may differ across a population. In this setting we study the role of empathy-the capacity to form moral evaluations from another person's perspective. We show that empathy tends to foster cooperation by reducing the rate of unjustified defection. The norms of moral evaluation previously considered most socially beneficial depend on high levels of empathy, whereas different norms maximize social welfare in populations incapable of empathy. Finally, we show that empathy itself can evolve through social contagion. We conclude that a capacity for empathy is a key component for sustaining cooperation in societies.
The data for all figures, code to produce the figures from these data, and the simulation code that generated the data are provided as Source data 1.
- Joshua B Plotkin
- Joshua B Plotkin
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
- Michael Doebeli, University of British Columbia, Canada
© 2019, Radzvilavicius et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
As an adapting population traverses the fitness landscape, its local neighborhood (i.e., the collection of fitness effects of single-step mutations) can change shape because of interactions with mutations acquired during evolution. These changes to the distribution of fitness effects can affect both the rate of adaptation and the accumulation of deleterious mutations. However, while numerous models of fitness landscapes have been proposed in the literature, empirical data on how this distribution changes during evolution remains limited. In this study, we directly measure how the fitness landscape neighborhood changes during laboratory adaptation. Using a barcode-based mutagenesis system, we measure the fitness effects of 91 specific gene disruption mutations in genetic backgrounds spanning 8000–10,000 generations of evolution in two constant environments. We find that the mean of the distribution of fitness effects decreases in one environment, indicating a reduction in mutational robustness, but does not change in the other. We show that these distribution-level patterns result from differences in the relative frequency of certain patterns of epistasis at the level of individual mutations, including fitness-correlated and idiosyncratic epistasis.
Despite decades of research, knowledge about the genes that are important for development and function of the mammalian eye and are involved in human eye disorders remains incomplete. During mammalian evolution, mammals that naturally exhibit poor vision or regressive eye phenotypes have independently lost many eye-related genes. This provides an opportunity to predict novel eye-related genes based on specific evolutionary gene loss signatures. Building on these observations, we performed a genome-wide screen across 49 mammals for functionally uncharacterized genes that are preferentially lost in species exhibiting lower visual acuity values. The screen uncovered several genes, including SERPINE3, a putative serine proteinase inhibitor. A detailed investigation of 381 additional mammals revealed that SERPINE3 is independently lost in 18 lineages that typically do not primarily rely on vision, predicting a vision-related function for this gene. To test this, we show that SERPINE3 has the highest expression in eyes of zebrafish and mouse. In the zebrafish retina, serpine3 is expressed in Müller glia cells, a cell type essential for survival and maintenance of the retina. A CRISPR-mediated knockout of serpine3 in zebrafish resulted in alterations in eye shape and defects in retinal layering. Furthermore, two human polymorphisms that are in linkage with SERPINE3 are associated with eye-related traits. Together, these results suggest that SERPINE3 has a role in vertebrate eyes. More generally, by integrating comparative genomics with experiments in model organisms, we show that screens for specific phenotype-associated gene signatures can predict functions of uncharacterized genes.