Overview
My research investigates how conserved signaling networks integrate environmental cues to regulate genome stability, morphogenesis, stress adaptation, and virulence in fungal pathogens. Using molecular genetics, functional genomics, proteomics, and quantitative imaging, I examine how kinase–phosphatase signaling pathways are rewired in pathogenic contexts to control infection-relevant cellular behaviors.
During my Ph.D. at the University of New Orleans, I developed a strong foundation in fungal genetics by studying nutrient sensing, mitochondrial biogenesis, and growth regulation in the budding yeast Saccharomyces cerevisiae. I identified novel regulatory roles for the kinase Sch9 within TORC1 and Ras/PKA signaling pathways and uncovered genetic links between mitochondrial function and metabolic control. This work established my foundation in eukaryotic signaling and genetic interactions.
As a postdoctoral associate in the Heitman laboratory at Duke University, I have led the first comprehensive functional characterization of the conserved Striatin-interacting phosphatase and kinase (STRIPAK) complex in the human fungal pathogen Cryptococcus neoformans. My work demonstrates that STRIPAK acts as a central signaling hub controlling genome stability, stress responses, sexual development, and virulence through subunit-specific regulatory mechanisms. Ongoing studies define how STRIPAK-dependent phosphorylation networks and genome plasticity promote fungal adaptation during host-associated stress.
Together, these studies form the foundation for an independent research program aimed at uncovering how conserved signaling complexes govern cellular decision-making in fungal pathogens and identifying fungal-specific regulatory vulnerabilities with relevance to antifungal intervention.