Social dominance hierarchy type and rank contribute to phenotypic variation within cages of laboratory mice.

A tacit assumption in laboratory animal research is that animals housed within the same cage or pen are phenotypically more similar than animals from different cages or pens, due to their shared housing environment. This assumption drives experimental design, randomization schemes, and statistical analysis plans, while neglecting social context. Here, we examined whether a domain of social context-social dominance-accounted for more phenotypic variation in mice than cage-identity. First, we determined that cages of mice could be categorized into one of three dominance hierarchies with varying degrees of dominance behavior between cage-mates, and low levels of agonistic behavior in the home-cage. Most groups formed dynamic hierarchies with unclear ranks, contrasting with recent accounts of stable transitive hierarchies in groups of mice. Next, we measured some phenotypic traits, and found that social dominance (i.e. dominance hierarchy type and degree of dominance behavior) consistently accounted for some phenotypic variation in all outcome measures, while cage-identity accounted for phenotypic variation in some measures but virtually no variation in others. These findings highlight the importance of considering biologically relevant factors, such as social dominance, in experimental designs and statistical plans.

No evidence for kin protection in the expression of sickness behaviors in house mice.

When infected, animals change their behaviors in several ways, including by decreasing their activity, their food and water intake, and their interest in social interactions. These behavioral alterations are collectively called sickness behaviors and, for several decades, the main hypotheses put forward to explain this phenomenon were that engaging in sickness behaviors facilitated the fever response and improved the likelihood of host survival. However, a new hypothesis was recently proposed suggesting that engaging in sickness behaviors may serve to protect kin. We tested this kin protection hypothesis by combining a field and a laboratory experiment in house mice. In both experiments, we induced sickness behaviors by administration of a pro-inflammatory agent. In the field experiment, we then collected genetic data and assessed whether relatedness affected the intensity of sickness behaviors. In the lab experiment, we manipulated relatedness in small social groups and assessed whether having a closely related individual (a sibling) in the group altered social interactions or visits to common resources (such as food and water containers) once immune-challenged. Our results do not support the kinship protection hypothesis and therefore advance our understanding of why such an apparently costly set of behavioral changes would be evolutionarily maintained.