My research focuses on the biology of genomic conflicts and what they can tell us about the evolution of conflict and cooperation more generally.
I develop population genetic theory and perform comparative analyses to ask how and why such conflicts occur and how they fit into models of social evolution. I also work on the foundations of the so-called gene’s-eye view of evolution, also known as selfish gene theory. I wrote a book on its history and development for Oxford University Press (published in 2021).
Mother’s Curse and Father’s Curse
The conflict between maternally inherited mitochondrial and bi-parentally inherited nuclear genes is one of the best described genomic conflicts in biology. Because genes in the mitochondrial genome are strictly maternally inherited, mutations that are beneficial in females can spread in a population even if they are deleterious in males. This is the Mother’s Curse.
With Andy Clark and Manisha Munasinghe (Cornell), I have used population genetic theory to show how the fate of compensatory nuclear modifier loci that alleviate the effect in males depend on whether they are located on autosomes or sex chromosomes. Our analytical framework also allowed us to discover a novel kind of sexual conflict: Father’s Curse. A major focus of current work is to determine how likely we should be to detect it nature. We are also using experimental crosses in Drosophila to test the extent of mitochondrial-Y chromosome epistatsis.
What can selfish genetic elements tell us about the evolution of conflict and cooperation?
I study what genomic conflicts have in common with other examples of conflict, whether spread of cancer cells, conflicts between worker ants over reproduction, or between the microbiome and its host organism. Together with Kevin Foster (University of Oxford) and With Nick Davis (LSHTM), I recently published a manuscript describing how enforcement, mechanisms that suppress selfish behaviour, is an underappreciated, and often critical, ingredient for cooperation at all levels of life – from genomes, eukaryotic cells and multicellular organisms to societies and mutualisms between species.
With Manus Patten I work on the so-called paradox of the organism. This is the fact that despite the opportunity for agents like selfish genetic elements and cancer cells to erode the organism from within, they usually do not. But why not? We were recently awarded a $250,000 grant over three years from the John Templeton Foundation to formally address this. We will be hiring a postdoc and organize a conference on the topic.
The foundations of the gene’s-eye view of evolution
For the past half century, the study of social evolution has benefited greatly by the so-called gene’s-eye view of evolution. Indeed, the gene’s-eye view was instrumental in bringing selfish genetic elements to the forefront of evolutionary biology and genetics. I am interested in the history of the gene’s-eye view of evolution, especially its relationship with the empirical study of selfish genetic elements (see also here and here).
Why are transposable elements so common, and the genomes so large, in some species but not in others?
Transposable elements are selfish genetic elements that can self replicate and insert into new locations in the genome. My PhD work with Stephen Wright (University of Toronto) centered on how changes in modes of inheritance, such as the evolution selfing, sex, and increases in ploidy, affect the evolutionary dynamics of transposons. I am also interested in how transposons contribute to variation in genome size, particularly in plants. I have studied these questions in a variety of plant systems, including Arabidopsis, Capsella, and Oenothera.