Why Candida albicans Filaments Better Than Its Budding Cousin
Candida albicans and C. dubliniensis are closely related pathogenic yeasts. However C. albicans exhibits greater virulence and an increased capacity to undergo filamentation (thus forming hyphae) both in vitro and in vivo. O'Connor et al. (p. 1383–1397) show that the increased morphological flexibility of C. albicans is due to its ability to filament regardless of nutrient availability. In both species, filament extension is driven by the transcriptional regulator UME6, and in C. dubliniensis, peptone was shown to reduce UME6 expression and filamentation. Strikingly, preculture of C. dubliniensis in a peptone-free synthetic medium enhanced subsequent filamentation and increased virulence. This research suggests that the increased virulence of C. albicans may be due to its ability to filament in a more diverse range of host environmental conditions.
Linking Transcriptional Regulation to Hyphal Development Mechanisms in Fungi
The ability to form and extend hyphal filaments is important for a wide variety of processes in pathogenic and nonpathogenic fungi, including nutrient scavenging, virulence, tissue invasion, and lysis of macrophages. Although numerous transcriptional regulators which respond to filament-inducing signals have been identified, the precise mechanisms by which these regulators control hyphal growth have largely remained elusive. In this issue, Carlisle and Kadosh (p. 1320–1328) demonstrate that Ume6, a key filament-specific transcriptional regulator in Candida albicans, drives hyphal growth via a mechanism involving the Hgc1 cyclin-related protein. The Hgc1/Cdc28 cyclin/Cdk complex is known to promote hyphal development by septin phosphorylation, inhibition of cell separation, and activation of the Cdc42 master polarity regulator. These findings are significant given that regulatory circuits and downstream mechanisms important for controlling morphogenesis are likely to be conserved in a wide variety of fungal species.