Group size is an important trait for many ecological and evolutionary processes. However, it is not a trait possessed by individuals but by social groups, and as many genomes contribute to group size understanding its genetic underpinnings and so predicting its evolution is a conceptual challenge. Here I suggest how group size can be modelled as a joint phenotype of multiple individuals, and so how models for evolution accounting for indirect genetic effects are essential for understanding the genetic variance of group size. This approach makes it clear that (a) group size should have a larger genetic variance than initially expected as indirect genetic effects always contribute exactly as much as direct genetic effects and (b) the response to selection of group size should be faster than expected based on direct genetic variance alone as the correlation between direct and indirect effects is always at the maximum positive limit of 1. Group size should therefore show relatively rapid evolved increases and decreases, the consequences of which and evidence for I discuss.

Diverse plants and animals have evolved specialized structures to filter and house beneficial microbes. These symbiotic organs form crucial points of exchange between host and symbiont, are often shaped by both partners, and exhibit features that facilitate a suite of microbial services. While symbiotic organs exhibit varied function, morphology, and developmental plasticity, they share core features linked to the evolutionary maintenance of beneficial symbiosis. Moreover, these organs can have a significant role in altering the demographic forces that shape microbial genomes, driving population bottlenecks and horizontal gene transfer (HGT). To advance our understanding of these \'joint phenotypes\' across varied systems, future research must consider the emergent forces that can shape symbiotic organs, including fitness feedbacks and conflicts between interacting genomes.

Evolutionary conflict and arms races are important drivers of evolution in nature. During arms races, new abilities in one party select for counterabilities in the second party. This process can repeat and lead to successive fixations of novel mutations, without a long-term increase in fitness. Models of co-evolution rarely address successive fixations, and one of the main models that use successive fixations-Fisher\'s geometric model-does not address co-evolution. We address this gap by expanding Fisher\'s geometric model to the evolution of joint phenotypes that are affected by two parties, such as probability of infection of a host by a pathogen. The model confirms important intuitions and offers some new insights. Conflict can lead to long-term Sisyphean arms races, where parties continue to climb toward their fitness peaks, but are dragged back down by their opponents. This results in far more adaptive evolution compared to the standard geometric model. It also results in fixation of mutations of larger effect, with the important implication that the common modeling assumption of small mutations will apply less often under conflict. Even in comparison with random abiotic change of the same magnitude, evolution under conflict results in greater distances from the optimum, lower fitness, and more fixations, but surprisingly, not larger fixed mutations. We also show how asymmetries in selection strength, mutation size, and mutation input allow one party to win over another. However, winning abilities come with diminishing returns, helping to keep weaker parties in the game.

Multiple organisms can sometimes affect a common phenotype. For example, the portion of a leaf eaten by an insect is a joint phenotype of the plant and insect and the amount of food obtained by an offspring can be a joint trait with its mother. Here, I describe the evolution of joint phenotypes in quantitative genetic terms. A joint phenotype for multiple species evolves as the sum of additive genetic variances in each species, weighted by the selection on each species. Selective conflict between the interactants occurs when selection takes opposite signs on the joint phenotype. The mean fitness of a population changes not just through its own genetic variance but also through the genetic variance for its fitness that resides in other species, an update of Fisher\'s fundamental theorem of natural selection. Some similar results, using inclusive fitness, apply to within-species interactions. The models provide a framework for understanding evolutionary conflicts at all levels.