Competition is inevitable in polymicrobial communities, where microbes share similar niches and must evolve strategies to secure resources or space. While interbacterial competition is well studied—often involving toxins or nutrient sequestration—less is known about how bacteria compete with fungi. Do bacteria use different molecular arsenals against fungal competitors? And how can we identify these mechanisms systematically?

We view microbial competition as a genetic conflict, where one species expresses an "offense" gene to antagonize another, which must protect itself either by evasion or by expressing a "defense" gene. Using this framework and a genome-wide bacterial fitness screen, we previously discovered that the human fungal pathogen Candida albicans sequesters Mg2+ to suppress the growth of the human bacterial pathogen Pseudomonas aeruginosa. This nutritional competition for Mg2+ is a widespread mode of competition between multiple fungi and gram-negative bacteria.

Building on this foundation, we are interested in understanding the mechanisms through which other Pseudomonas species engage in fungal competition, how diverse fungal species mount defense, and how bacteria and fungi adapt in this arms race.

Our previous work revealed that fungal-bacterial competition for Mg2+ alters bacterial adaptation to antibiotics. This indicates that competition may broadly impact how microbes respond or adapt to other stressors, such as host immune defense during infection.

To explore this further, we use plant and animal infection models combined with microbial genetics and genomics, and cell biology experiments. We aim to identify fungal and bacterial genes critical for polymicrobial infections and to understand how cross-kingdom microbial interactions drive the progression of infectious diseases and host response. Ultimately, our goal is to understand how these interactions shape microbial virulence and adaptation in complex, host-associated ecosystems.