A dynamic genome with high plasticity contributes directly to the success of the organism to adapt to changing environments. My lab studies genetic mechanisms that sustain structural and functional flexibility while maintaining the integrity of the organism using the model fungal system Fusarium oxysporum.
F. oxysporum is a highly adaptive species complex that consists of both plant and human pathogens. Collectively, members within this species complex cause destructive and intractable wilt diseases across a diverse spectrum of plant hosts, including numerous economically important crops: e.g., cotton, canola, melons, and tomato. During the past two decades, F. oxysporum strains have also emerged as opportunistic pathogens causing life-threatening infections in immunocompromised patients. However, any single pathogenic form exhibits strong host specificity. Comparative genomics demonstrated that horizontal transfer of pathogenicity chromosomes conveys host-specific pathogenicity (Ma et al., 2010). The pathogenicity chromosomes encoded in each pathogenic form provide a focal point for investigating the genetic mechanisms that underlie pathogenesis. F. oxysporum has also been used to study host-pathogen interactions to investigate horizontal chromosome transfer in eukaryotes.