The relationship between robustness and evolution

Jiang, P.; Kreitman, M.; Reinitz, J.

doi:10.1101/268862

Home/Archive/bioRxiv

bioRxiv · 10.1101/268862

The relationship between robustness and evolution

Jiang, P.·Kreitman, M.·Reinitz, J.

View original source ↗Export metadata ↓

Abstract

Canalization involves mutational robustness, the lack of phenotypic change as a result of genetic mutations. Given the large divergence in phenotype across species, understanding the relationship between high robustness and evolvability has been of interest to both theorists and experimentalists. Although canalization was originally proposed in the context of multicellular organisms, the effect of multicellularity on evolvability has not been considered by theoreticians. We address this issue using a Boolean population model with explicit representation of an environment in which multicellular individuals with explicit genotype and phenotype evolve. Robustness is described by a single real number between zero and one. We find that high robustness is favored in constant environments, and lower robustness is favored after environmental change. Multicellularity severely constrains robustness: peak evolvability occurs at an absolute level of robustness of about 0.99 compared with values of about 0.5 in a classical neutral network model. Multicellularity results in a sharp peak of evolvability in which the maximum is set by the fact that the fixation of adaptive mutations becomes more improbable as robustness decreases. When robustness is put under genetic control, robustness levels leading to maximum evolvability are selected for, but maximal relative fitness appears to require recombination.

Explore related subjects

evolutionary biology Preprint

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

Jiang, P., Kreitman, M., Reinitz, J.. 2018-02-22. The relationship between robustness and evolution. https://doi.org/10.1101/268862

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

bioRxiv2026

A Deep Phylogenetic Split Between Short- and Long-Wavelength-Tuned Visual Systems in Surgeonfishes (Acanthuridae)

The light environment, coupled with ecology, is widely thought to drive visual adaptation, creating species-specific visual niches. However, coral reef ecosystems experience continuous spatiotemporal variations in light conditions, and mechanisms such as phenotypic plasticity may be essential for coral reef animals to adjust to such changing sensory requirements. It remains unclear how widespread colour vision plasticity is, or the extent to which ecology and phylogeny drive plasticity in coral reef fishes. Using a comparative transcriptomic approach across 22 species, we aimed to investigate visual plasticity within a prominent coral reef fish family, surgeonfishes (Acanthuridae), in response to changes in the light environment throughout development and across seasons in adults. Surprisingly, we uncovered a deep phylogenetic split (~42 mya) in visual opsin gene expression profiles, with Nasinae expressing a shorter-shifted palette than Acanthurinae, which coincides with the divide between water-column and benthic-feeding modalities during the speciation of their last common ancestor. However, opsin gene expression showed little variation in response to seasonal or ontogenetic shifts in the light environment, nor in the broad functional feeding groups extant species from both subfamilies fall under. Thus, the invariable visual gene expression observed in present-day surgeonfishes appears to be dictated by phylogenetic inertia, despite rapid diversification into a range of ecological niches. This suggests that spectral tuning into two main modalities, short and long, reduces the need for visual plasticity, allowing larger and more mobile coral reef fishes to conduct visually guided behaviours across the entire range of light environments they encounter.

evolutionary biology↗

bioRxiv2026

Efficient growth factor production stabilizes cooperation in a cellular public goods game

Eukaryotic cells secrete growth factors that facilitate the proliferation and survival of neighboring cells in a coordinated manner essential for tissue development, repair, and homeostasis. However, mutant cells that fail to produce these factors may exploit the benefits provided by neighboring producers, thereby gaining a proliferative advantage that could lead to the extinction of the producer clone. Evolutionary theory predicts that preventing this "tragedy of the commons" requires a fixed spatial structure or other mechanisms that enable cells to interact preferentially with copies of themselves. Contrary to this expectation, we found that, in competition experiments, cells producing the diffusible growth factor interleukin-3 (IL3) resist invasion by non-producing mutant cells even in well-mixed populations, and that non-producers are driven to extinction instead. Using evolutionary game theory, we show that this outcome arises when the cost-to-benefit ratio of growth factor production falls below a critical threshold. We derive this tipping point analytically across the full parameter space of benefit function shape and group size and confirm that IL3 production in our experimental system satisfies this condition with a production cost less than 0.1% of the benefit conferred. These results demonstrate that efficient public good production alone can resolve the tragedy of the commons in populations of cells, and potentially in other biological systems.

evolutionary biology↗

bioRxiv2026

Repeated Transitions in Migratory Behavior Across a Songbird Radiation Are Not Driven by Selection on Shared Variation in Candidate Genes

Understanding the mechanisms facilitating the repeated evolution of traits is a core question in evolutionary biology. While repeated evolution has been observed across many systems, behavioral phenotypes have been less well studied than morphological traits. Migration is a behavioral adaptation to seasonality that has evolved independently in many animals, and repeated gains and losses of migratory behavior have been especially prevalent throughout the diversification of birds. While migratory traits are heritable in many taxa and candidate genes underlying intraspecific variation in migratory behavior have been identified, whether similar genetic changes are responsible for the repeated evolution of migration remains poorly understood. We used a phylogenomic approach to investigate the relationship between variation in candidate genes and migratory propensity across nearly all species in the parulid warbler radiation (n = 101), a group of songbirds in which migratory behavior has been lost and gained multiple times. Comparisons of candidate gene tree topologies to the parulid warbler species tree revealed cases of discordance, though these were explained by differences in the number of phylogenetically informative sites among genes rather than by elevated genetic similarity among species sharing migratory strategies. Testing models of coding sequence evolution identified sites with elevated dN/dS in five candidate genes, suggestive of positive selection; however, variation at these sites showed no clear association with migratory strategy, nor did we detect recurrent selection across lineages where transitions in migratory behavior most likely occurred. Together, these results contradict the hypothesis that selection on shared variation (ancestral polymorphisms or introgressed alleles) facilitated the repeated evolution of migration in this clade.

evolutionary biology↗