Past studies examining the disease costs of sociality have generally explored hypotheses that link larger group size to higher rates of infection transmission. However, beyond a simple dependence on group size, infection spread is largely influenced by the organization of infection-spreading interactions between individuals.
The success of symmetries in explaining the physical world, from general relativity to the standard model of particle physics and all phases of matter, raises the question of why the same concept could not be equally applied to explain emergent properties of biological systems.
Embryonic development generates a variety of complex organisms using diverse and contrasting developmental strategies. For instance, adaptation to seasonal drought by annual killifish leads to a unique developmental pattern in which embryogenesis occurs only after undifferentiated embryonic cells have completed epiboly and dispersed at low density on the egg surface (Fig 1A). Hence, the first stage of embryogenesis requires congregation of embryonic cells to form a single aggregate that gives rise to the embryo proper. How embryonic cells do this is currently unknown.
Sleep periods exhibit numerous intermittent transitions among sleep stages and short awakenings, with fluctuations within sleep stages that may trigger micro-states and arousals. Despite the established association between dominant brain rhythms and emergent sleep stages, origin and functions of sleep-arousals and sleep-stage transitions remain poorly understood.