Butterflies and moths (the order Lepidoptera) account for around 10% of the described animal species and play important ecological and economic roles. They also show an extraordinary diversity in chromosome structure. However, this diversity is unevenly distributed across the lepidopteran phylogeny. While most species have retained the ancestral lepidopteran karyotype of 31 chromosomes, a small number of lineages have undergone extensive chromosomal rearrangement. Using more than 1,200 chromosome-level genomes generated by Project Psyche and the Darwin Tree of Life Project, I investigate why some lineages experience rapid chromosomal change while others remain remarkably stable, and what this means for speciation.
Identifying drivers of chromosomal rearrangement
A central question in my work is whether the causes of large-scale genome rearrangements can be inferred from patterns of base substitution. Mutations leave characteristic “signatures” that reflect the source of DNA damage and the cellular pathways that repair it. Mutational signature analysis has become a powerful approach for identifying the causes of human cancers but has rarely been applied across the tree of life. Because chromosomal rearrangements also arise from DNA damage and misrepair, I am applying this approach across Lepidoptera to ask whether lineages with unusually high rates of chromosomal rearrangement also show distinctive mutational spectra.
I also ask whether defensive compounds used by Lepidoptera alter these mutational spectra. Many butterflies and moths sequester or synthesise chemically diverse compounds for defence, some of which are known to damage DNA in model organisms. This raises the possibility that the chemicals butterflies have evolved to use for defence may themselves influence genome evolution. I am testing whether exposure to these naturally occurring toxins leaves detectable signatures in the genomes of Lepidoptera, and whether lineages exposed to them show elevated rates of chromosomal rearrangement. Together, these mutational signatures could help identify causes of both nucleotide-level mutations and chromosomal rearrangements, including oxidative damage, chemical exposure, or defects in meiotic repair.
Consequences of chromosomal rearrangement for speciation
I am equally interested in what happens after chromosomal rearrangements arise. Can they help populations become reproductively isolated and contribute to speciation? The Neotropical butterfly tribe Ithomiini provides a natural system for addressing this question. Some Ithomiini genera have speciated rapidly in the past million years, whereas their close relatives have speciated at a more normal rate for Lepidoptera. Across a suture zone in the Peruvian Andes, many karyotypically divergent Ithomiini populations meet and hybridise. Using chromosome-level pangenomic assemblies and analyses of introgression, I am testing whether gene flow is reduced around chromosomal rearrangement breakpoints.
What draws me to this work is the combination of field, laboratory, and computational approaches, and the opportunity to move across scientific fields to understand how changes in genome architecture arise and how they can shape the evolution of new species; from chemical ecology and mutational biology, through chromosome evolution and population genetics, to speciation.
My timeline
PhD Student at the Wellcome Sanger Institute, University of Cambridge
MSc Bioinformatics, Wageningen University & Research
Research Intern in the Hochberg Group, Max Planck Institute for Terrestrial Microbiology
MSc Thesis Supervised by Prof. Schranz and Dr. Bakker, Wageningen University & Research
BSc Plant Sciences, Wageningen University & Research
BSc Thesis Supervised by Prof. Trindade and Dr. Pancaldi, Wageningen University & Research