Candidiasis represents the fourth most frequent nosocomial infection both in the US and worldwide. C. albicans is the most common cause of candidiasis which has unacceptably high morbidity and mortality rates and important economic repercussions (estimated total direct cost of approximately 2 billion dollars in 1998 in US hospitals alone). The pathogenic potential of C. albicans is intimately related to certain key processes including biofilm formation and filamentation. C. albicans can grow as yeast cells, pseudohyphae or hyphae and produce chlamydospores with its form being dictated by its surrounding conditions. The ability to form hyphal cells has been fundamentally linked to the disease potential of this organism. In fact, cells which cannot make this transition are avirulent. NRG1p is a global repressor of the filamentation process of C. albicans and associates with the co-repressor Tup1p during this inhibition of filamentation. NRG1p has also been shown to play a key role in chlamydospore formation, but the relevance of Tup1p is unknown. This study uses mutant strains and quantitative real-time PCR to analyze the roles of Tup1p and select hyphal specific genes in chlamydospore formation. We describe differences in the nature of NRG1p regulation of chlamydospore formation compared to filamentation and offer further insights into NRG1p function in Candida albicans. Furthermore, we establish that chlamydospore formation is independent of Tup1p.