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• Cellular and developmental biologybof infection-related morphogenesis in fungal pathogens
  
• Molecular basis and regulation of fungal pathogenesis

My research group explores the basic molecular-genetic mechanisms underlying fungal pathogenesis. The long-term goal being the elucidation of specific developmental and physiological programs evolved by fungal pathogens to infect and colonize host tissues. Presently, we utilize the blast fungus Magnaporthe grisea, and its host Rice, as a model pathosystem for understanding fungal virulence and host specificity. We rely on molecular genetics, cell biology, biochemistry and functional genomics as tools to understand the molecular and regulatory basis of the infection-related development in fungal pathogens and to elucidate the underlying basis of the fungus-host interactions.

A novel forward-genetics approach to identify mutant derivatives of the blast fungus was highly successful and yielded 24 non-pathogenic mutants in our primary screening process. The research is currently focused on functional characterization of these mutants, that represent non-allelic lesions in pathways controlling host surface sensing, cytoskeletal dynamics, signal transduction, osmoregulation, peroxisome biogenesis, membrane resealing, ion homeostasis, targeted secretion etc. We also study the primary and secondary metabolism associated with fungal virulence, and the host-specific regulation of these metabolic events during plant disease.

Figure 1: The DIC and DAPI-stained hyphal filaments and the asexual conidia of Magnaporthe are depicted along with the full-blown blast disease symptoms on rice leaves. The key steps in the pathogenic cycle of Magnaporthe that formed the basis of our forward genetics approach are marked (X) and the categories of mutants screened for are listed, The lowest panels depict the mutant characterization which includes evaluating disease symptoms and infection related morphogenesis in the mutant and the complemented strain (rescued) as compared to the wild-type.