Temperature change is a ubiquitous environmental signal, which exerts powerful control over the development and virulence of microbial pathogens. For Candida albicans, the leading fungal pathogen of humans, temperature influences mating, phenotypic switching, resistance to antifungal drugs and the morphogenetic transition from yeast to filamentous growth. C. albicans morphogenesis is profoundly influenced by temperature, and most filament-inducing cues depend on a concurrent increase in temperature to 37°C before morphogenesis can occur, although the molecular mechanisms underpinning this temperature-dependent developmental transition remain largely unknown. We established that the thermally responsive molecular chaperone Hsp90 orchestrates temperature-dependent morphogenesis, via previously uncharacterized cellular circuitry, comprised of the cyclin-dependent kinase Pho85, the cyclin Pcl1 and the transcriptional regulator Hms1. Here we elaborate on Hsp90's pleiotropic effects on temperature-dependent morphogenetic circuitry, and highlight how changes in protein form and function in response to stress complements the diverse repertoire of mechanisms of microbial temperature sensing.