One of the most fascinating questions in evolutionary biology is how genuinely new structures arise. Most phenotypic evolution consists of gradual modifications of pre-existing traits, but occasionally innovations appear that have no clear homolog in their ancestors — and these novelties often open up entirely new evolutionary possibilities. How are such structures built from inherited developmental programmes and genomic toolkits? What kinds of genomic change — regulatory rewiring, co-option of pre-existing gene networks, emergence of new genes — enable their origin?

To address these questions, our lab combines comparative multi-omics (genomics, transcriptomics, epigenomics) with developmental biology tools to reconstruct the evolutionary history of key morphological innovations. We work with two complementary model systems: on the one hand, the turtle carapace, a structure entirely unique among vertebrates whose developmental basis remains poorly understood; and on the other, the endothelium — and its haemogenic capacity during embryonic development —, a key vertebrate novelty that offers a window into the invertebrate-to-vertebrate transition and the origin of haematopoiesis. We apply state-of-the-art single-cell and spatial transcriptomics to characterize the gene regulatory networks active during the development of these structures, and to identify the genomic changes that enabled their origin and diversification.

A central question in our lab is how whole-genome duplications (WGDs) have shaped the phenotypic evolution of vertebrates. WGDs are a recurrent feature of vertebrate genome history: gnathostomes (jawed vertebrates) and cyclostomes (jawless fishes) share an ancestral duplication (1R), while gnathostomes underwent a second round (2R) and cyclostomes experienced an independent triplication after their split from the former (CR). And yet, a striking puzzle remains: despite comparable levels of genome duplication, gnathostomes have diversified into the immense morphological variety we see today, while cyclostomes have not. Why?

To address this question, we are sequencing and analysing new cyclostome genomes, with a particular focus on unravelling the architecture and consequences of this group’s specific triplication. By comparing genomes, transcriptomes, and epigenomes, we investigate how duplicated genes are retained, lost, or acquire new functions; how regulatory landscapes expand or contract; and how these molecular changes translate — or do not — into morphological innovation. Our goal is to understand the mechanistic and historical link between genome architecture and phenotypic diversification, using cyclostomes as a unique natural experiment in evolutionary genomics.