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We have focused our recent studies on the identification of functional pathways required for resistance to Nikkomycin Z (NZ), an antifungal agent that inhibits cell wall chitin biosynthesis in budding yeast. Unlike wild-type cells that are relatively resistant to NZ (IC50=25mm), most myosin II-deficient (myo1D) strains of yeast Saccharomyces cerevisiae require chitin synthesis for survival and are hypersensitive to very low concentrations of NZ (IC50=6.25 mm). Through the use of genetics we are interested in identifying which functional pathways interact (indirectly or directly) with Myo1p in this hypersensitivity phenotype and thereby identify how myosin II functions can be related to cell wall integrity. We believe that what we learn about the mechanism of resistance to NZ in myo1D strains may be applicable to other antifungal drugs that target cell wall synthesis.