In the elegant symmetry of Mendelian genetics, each allele is promised an equal chance at inheritance. But biology doesn’t always play fair. Meiotic drive subverts this balance, allowing selfish genetic elements to cheat the rules and bias their transmission to the next generation. For example, some drivers kill the gametes that don’t carry them, spreading through populations despite harming fertility. By violating Mendel’s law of equal segregation, they ignite internal genetic conflicts that can reshape genomes, disrupt reproductive systems, and drive evolutionary innovation. In our lab, we study these molecular cheaters—not just to understand how they bend the rules, but to uncover how host genomes fight back and their impact on genome and cellular evolution.

How can genes so vital change so quickly? This paradox lies at the heart of our curiosity. We propose that the answer is rooted in genetic conflict. Many rapidly evolving essential genes aren’t just performing routine cellular tasks—they are engaged in an ongoing battle against selfish genetic elements, such as meiotic drivers and transposons, or even external pathogens like bacteria and viruses. In this evolutionary arms race, rapid change is a survival strategy.

Just as a wound invites healing and transformation, the pressure from these genetic conflicts forces essential genes to adapt and evolve. These adaptations may rewire regulatory networks, reshape chromatin dynamics, or give rise to entirely new genes. In our lab, we aim to uncover the molecular scars and innovations left behind by these conflicts—to understand how they shape genome architecture, influence fertility, and drive the evolution of fundamental biological processes.

Currently, we focus on a group of rapidly evolving essential genes, sperm nuclear proteins (or protamines), which replace histones to pack DNA in sperm nuclei. 

While most cells in an organism typically share the same set of chromosomes, there are notable exceptions. A familiar example is the sex chromosomes: males typically carry one X and one Y chromosome, while females carry two X chromosomes. Beyond this, some species harbor extra chromosomes known as B chromosomes or possess chromosomes limited to specific tissues or stages of development, such as germline-restricted chromosomes. These chromosomes often defy the expectations of Mendel’s laws, which predict equal segregation and inheritance from both parents. These "genomic outlaws" often evolve selfish behaviors to manipulate cell division and ensure their own transmission.

By investigating these atypical chromosomes and their unusual selfish behaviors, we aim to understand how chromosomes evolve under non-Mendelian inheritance and how organisms preserve genomic integrity while managing such exceptions. This work will not only reveal fundamental principles of chromosome biology but will also shed insight into the origins and therapies of chromosomal abnormalities in cancer cells.