Understanding epidemic dynamics has always been a challenge. As witnessed from the ongoing Zika or the seasonal Influenza epidemics, we still need to improve our analytical methods to better understand and control epidemics. While the emergence of complex sciences in the turn of the millennium have resulted in their implementation in modelling epidemics, there is still a need for improving our understanding of critical dynamics in epidemics. In this study, using agent-based modelling, we simulate a Susceptible-Infected-Susceptible (SIS) epidemic on a homogeneous network. We use transfer entropy and active information storage from information dynamics framework to characterise the critical transition in epidemiological models. Our study shows that both (bias-corrected) transfer entropy and active information storage maximise after the critical threshold ( $R_0$ = 1). This is the first step toward an information dynamics approach to epidemics. Understanding the dynamics around the criticality in epidemiological models can provide us insights about emergent diseases and disease control.

The migration of people between different cultures has affected cultural change throughout history. To understand this process, cross-cultural psychologists have used the ‘acculturation’ framework, classifying ‘acculturation orientations’ along two dimensions: the willingness to interact with culturally different individuals, and the inclination to retain the own cultural identity (‘cultural conservatism’). Here, using a cultural evolution approach, we construct a dynamically explicit model of acculturation. We show that the evolution of a multicultural society, where immigrant and resident culture stably coexist, is more likely if individuals readily engage in cross-cultural interactions, and if resident individuals are more culturally conservative than immigrants. This result holds if some cultural traits pay off better than others, and individuals use social learning to adopt more advantageous cultural traits. Our study demonstrates that formal dynamic models can help us understand how individual orientations towards immigration eventually determine the population-level distribution of cultural traits.

Multicellularity evolved independently in multiple lineages, yielding organisms with a wide range of adult sizes. Building an intact soma is not a trivial task, when dividing cells accumulate damage. Here, we study “ontogenetic management strategies,” that is rules of dividing, differentiating and killing somatic cells, to examine two questions: first, do these rules evolve differently for organisms differing in the target mature body size, and second, how well a strategy evolved in small‐bodied organisms performs if implemented in a large body—and vice versa (“large”‐evolved strategies in small bodies). We model the growth and mature lifespan of an organism starting from a single cell and optimize, using a genetic algorithm, trait combinations across a range of target sizes, with seven evolving traits: (a) probability of asymmetric division, (b) probability of differentiation (per symmetric cell division), (c) Hayflick limit, (d) damage response threshold, (e) damage response strength, (f) number of differentiation steps and (g) division propensity of cells relative to “stemness.” Some but not all traits evolve differently depending on body size: large‐bodied organisms perform best with a smaller probability of differentiation, a larger number of differentiation steps on the way to form a tissue and a higher threshold of cellular damage to trigger cell death, than small organisms. Strategies evolved in large organisms are more robust: they maintain high performance across a wide range of body sizes, while those that evolved in smaller organisms fail when attempting to create a large body. This highlights an asymmetry: under various risks of developmental failure and cancer, it is easier for a lineage to become miniaturized (should selection otherwise favour this) than to increase in size.

The predominance of sexual reproduction in eukaryotes remains paradoxical in evolutionary theory. Of the hypotheses proposed to resolve this paradox, the ‘Red Queen hypothesis’ emphasises the potential of antagonistic interactions to cause fluctuating selection, which favours the evolution and maintenance of sex. Whereas empirical and theoretical developments have focused on host-parasite interactions, the premises of the Red Queen theory apply equally well to any type of antagonistic interactions. Recently, it has been suggested that early multicellular organisms with basic anticancer defences were presumably plagued by antagonistic interactions with transmissible cancers and that this could have played a pivotal role in the evolution of sex. Here, we dissect this argument using a population genetic model. One fundamental aspect distinguishing transmissible cancers from other parasites is the continual production of cancerous cell lines from hosts’ own tissues. We show that this influx dampens fluctuating selection and therefore makes the evolution of sex more difficult than in standard Red Queen models. Although coevolutionary cycling can remain sufficient to select for sex under some parameter regions of our model, we show that the size of those regions shrinks once we account for epidemiological constraints. Altogether, our results suggest that horizontal transmission of cancerous cells is unlikely to cause fluctuating selection favouring sexual reproduction. Nonetheless, we confirm that vertical transmission of cancerous cells can promote the evolution of sex through a separate mechanism, known as similarity selection, that does not depend on coevolutionary fluctuations.

Ubiquity of cancer across the tree of life yields opportunities to understand variation in cancer defences across species. Peto’s paradox, the finding that large-bodied species do not suffer from more cancer despite having more cells at risk of oncogenic mutations compared to small species, can be explained if large size selects for better cancer defences. Since birds live longer than non-flying mammals of equivalent size, and are descendants of moderate-sized dinosaurs, we ask whether ancestral cancer defences are retained if body size shrinks in a lineage. Our model derives selection coefficients and fixation events for changes in cancer defences over macroevolutionary time, based on known relationships between body size, cancer risk, extrinsic mortality, metabolic rate, and effective population size. We show that, if mutation rate is sufficiently high and cancer defences are costly, we expect birds to have lower cancer defences than their dinosaurian ancestors. However, if the evolution of cancer suppression is mutation limited, due to e.g. pleiotropy, birds may have kept excessive dinosaurian cancer defences, possibly explaining their low cancer risk. Counterintuitively, birds can then be ‘too robust’ for their own good, if excessive cancer suppression requires compromising reproductive rates. Yet, evolutionary innovations such as flight can increase longevity and keep selection for cancer suppression intact in birds, even if flight requires small body size. Retaining dinosaur-level cancer defences can then be adaptive, particularly if the evolution of flight is accompanied by an increase in cancer risk due to metabolic scaling. Overall, our study suggests that studying cancer suppression in birds can reveal alternative mechanisms to those found in mammals, possibly inherited from birds’ dinosaurian ancestors.