Most fungi related to systemic human infections are environmental pathogens that do not require the host to complete their normal life cycle. Much remains unknown regarding how and why pathogenicity has evolved in these environmental fungi. Our study is driven by those questions. Our model system is one of the most successful environmental pathogens, Cryptococcus neoformans, which is responsible for 1 million new infections and 600,000 deaths annually worldwide. My lab investigates fungal environmental adaptation strategies underlying cryptococcal pathogenicity, antifungal tolerance and the evolution of virulence. Our research focus on three areas:

(1) we study the key decision-making circuits engaged in the formation of different morphology subpopulations during sexual community differentiation or during disease progression.

(2) we explore novel fungal intercellular and intracellular signals, understanding their mechanisms of action.

(3) we unveil unique and widespread fungal environment sensing systems and explore their functional role in pathogenicity and antifungal tolerance.

(4) we identify the determinants of antifungal tolerance caused by host factors and develop new antifungal therapies.

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