Under basal conditions, HSF1 levels are moderate and C. albicans exists in the yeast form. A reduction in HSF1 levels leads to filamentous growth both by compromising Hsp90 function and through circuitry that is independent of Hsp90 but dependent on Efg1. An increase in HSF1 levels induces a dose-dependent expansion of Hsf1 direct targets that drives overexpression of positive regulators of morphogenesis, including Brg1 and Ume6, and decreased expression of negative regulators of morphogenesis, such as Nrg1, resulting in filamentous growth. Filaments induced by HSF1 overexpression and depletion are structurally distinct, require different genetic circuitry and are induced through distinct mechanisms.