The foundations of genomic complexity in multicellular animals have deep roots in their unicellular prehistory, both in terms of innovations in gene content, as well as the evolutionary dynamics of genome architecture.

Many different human cell lines, including both normal and cancer cells, appear to converge to a state that contains an unusual number of chromosomes when they are grown in culture.

Human cell lines regress to become ‘de-sexualized’ by reconfiguring to a 2:3 X/A ratio of high fitness, thus shedding light on the evolution of mammalian sex chromosomes.

Upon detecting a fatal infection using chemical cues, ants puncture the cuticle of sick brood and inject antimicrobial poison that disrupts the pathogen's life cycle and prevents it from reproducing, thus protecting the colony from disease.

Cancer is a consequence of the release of basal cellular functions inherited from our unicellular ancestors from the control of regulatory networks that evolved during the emergence of multicellularity.

Mathematical modeling shows that reproductive specialization is strongly favored in sparse networks of cellular interactions that reflect the morphology of early multicellular organisms, even when benefits of specialization are saturating.

Selection for undifferentiated multicellularity emerges in an evolutionary cell-based model because a collective of cells performs chemotaxis better than single cells in a noisy environment.

A new model describes evolutionary transitions in individuality in terms of tradeoff and tradeoff-breaking events as opposed to changes in the nature of fitness.