Evolution builds complexity at every scale. The diversification of species fills the living world with an extraordinary range of forms and adaptations. New genes and regulatory networks give rise to new functions and organs, enabling lineages to cross fundamental ecological boundaries and adopt radically different ways of life. In rare but transformative events, evolution produces an entirely new level of individuality — the superorganism, where most individuals no longer reproduce on their own but function as parts of a higher-level biological entity. Understanding how this complexity is generated, and what genomic changes underlie each step, is the central question of our lab.

Each of these steps poses its own evolutionary puzzle. Species diversify rapidly, but rapid radiation means that genomes share deep ancestral variation that was never fully sorted among descendant lineages, blurring the boundary between species histories and raising the question of whether traits we attribute to convergent evolution may instead reflect shared ancestry. When evolution does produce genuine novelty, a new organ, a new developmental programme, we want to know whether it was built from scratch or assembled by repurposing regulatory circuits that evolved for something else entirely. And when a new level of individuality emerges, we ask how a single genome came to encode the developmental capacity to produce radically different castes, and whether independent origins of superorganismality have converged on the same regulatory solutions. These questions span the tree of life, but their logic extends to our own species: the same evolutionary forces — conflict, trade-off, mismatch, and the legacy of selection acting differently across populations — shape human vulnerability to disease in ways that only an evolutionary framework can explain.

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