Steep Hierarchies without Skew? Modeling How Ecology and Decision-Making Shape Despotism of Relationships.

AbstractAnimals can form dominance relationships that vary from highly unequal, or despotic, to egalitarian, and this variation likely impacts the fitness of individuals. How and why these differences in relationships and fitness exist among groups, populations, and species has been the subject of much debate. Here, we investigated the influence of two major factors: (1) spatial resource distribution and (2) the presence or absence of winner-loser effects. To determine the effects of these factors, we built an agent-based model that represented 10 agents directly competing over food resources on a simple landscape. By varying the food distribution and using either asymmetry of strength or experience, we contrasted four scenarios from which we recorded attack decisions, fight outcomes, and individual energy intake to calculate dominance hierarchy steepness and energetic skew. Surprisingly, resource distribution and winner-loser effects did not have the predicted effects on hierarchy steepness. However, skew in energy intake arose when resources were distributed heterogeneously, despite hierarchy steepness frequently being higher in the homogeneous resource scenarios. Thus, this study confirms some decades-old predictions about feeding competition but also casts doubt on the ability to infer energetic consequences from observations of agonistic interactions.

The genetic basis of neurocranial size and shape across varied lab mouse populations.

Brain and skull tissues interact through molecular signalling and mechanical forces during head development, leading to a strong correlation between the neurocranium and the external brain surface. Therefore, when brain tissue is unavailable, neurocranial endocasts are often used to approximate brain size and shape. Evolutionary changes in brain morphology may have resulted in secondary changes to neurocranial morphology, but the developmental and genetic processes underlying this relationship are not well understood. Using automated phenotyping methods, we quantified the genetic basis of endocast variation across large genetically varied populations of laboratory mice in two ways: (1) to determine the contributions of various genetic factors to neurocranial form and (2) to help clarify whether a neurocranial variation is based on genetic variation that primarily impacts bone development or on genetic variation that primarily impacts brain development, leading to secondary changes in bone morphology. Our results indicate that endocast size is highly heritable and is primarily determined by additive genetic factors. In addition, a non-additive inbreeding effect led to founder strains with lower neurocranial size, but relatively large brains compared to skull size; suggesting stronger canalization of brain size and/or a general allometric effect. Within an outbred sample of mice, we identified a locus on mouse chromosome 1 that is significantly associated with variation in several positively correlated endocast size measures. Because the protein-coding genes at this locus have been previously associated with brain development and not with bone development, we propose that genetic variation at this locus leads primarily to variation in brain volume that secondarily leads to changes in neurocranial globularity. We identify a strain-specific missense mutation within Akt3 that is a strong causal candidate for this genetic effect. Whilst it is not appropriate to generalize our hypothesis for this single locus to all other loci that also contribute to the complex trait of neurocranial skull morphology, our results further reveal the genetic basis of neurocranial variation and highlight the importance of the mechanical influence of brain growth in determining skull morphology.