Broadly, I am interested in understanding the mechanisms that promote and limit the evolution of novel traits. Novelties (taxon-restricted features) can arise at all levels of biological organization – from the origin of new coding sequence to the elaboration of new multicellular structures. To develop a truly comprehensive understanding of the evolution of animal form and function, my lab studies everything from gene duplication to interspecific signaling systems. We work primarily with cnidarians (corals, jellies, and their allies) and ctenophores (comb jellies) but we never pass up the opportunity to study novel novelties.
The origin of new traits is one of the primary factors promoting the evolution of biodiversity. In the Babonis Lab, we use the dynamic processes of embryogenesis and tissue morphogenesis to understand how novel traits arise. One of our primary interests focuses on understanding the evolution of novel cell types, including the cnidocytes (“stinging” cells) of cnidarians. To dissect the evolutionary history of cnidocytes, we manipulate gene expression in vivo and employ diverse sequencing, imaging, and behavioral assays to characterize the phenotypic outcomes. Here’s a weird thought: trait loss is also an important driver of biodiversity. As part of our effort to understand how novelty promotes morphological and functional diversification, we also study the evolution of loss. Specifically, we investigate the fate of genes (and the cell lineages in which they are expressed) when they are released from their role in patterning lost structures. For example, by studying the function of colloblast (adhesive cell) genes in a ctenophore that no longer makes colloblasts, we aim to understand the evolution of novel gene regulatory networks.
Please see a current list of publications here.
In the news
- Babonis, et al., report: Single gene causes stinging cell to lose its sting
- Single gene causes stinging cell to lose its sting
- Jellyfish’s stinging cells hold clues to biodiversity