Until recently, the most commonly isolated human fungal pathogen, Candida albicans, was thought to be strictly asexual. But the recent discovery of a mating-type-like locus, shortly followed by proofs of mating, revised this classification and opened a new field of research in C. albicans. Based on data recently published by our group and others it is clear that the C. albicans version of the mating signaling cascade presents noticeable evolutionary differences with the well established Saccharomyces cerevisiae model. Because some of the mating-associated Mitogen-Activated Protein Kinase (MAPK) cascade components are shared among other signaling pathways, including the pathway directing hyphal formation known to be essential for C. albicans virulence, understanding the mating signaling cascade have implications beyond sexual reproduction.
Our current understanding of the mating MAPK cascade in C. albicans largely relies on the model established in the budding yeast S. cerevisiae. Briefly, following pheromone binding to the pheromone receptor, a sequentially-activated signaling cascade composed of a heterotrimeric G-protein complex (Gpa1p/Ste4p/Ste18p) and multiple MAPKs (Ste20p, Ste11p, Ste7p, Fus3p) will transduce the signal to the nucleus and trigger pheromone-mediated responses. Coordination and modulation of the mating-transducing signal primarily relies on two scaffold proteins Ste5p and Far1p, the former acting prior to the latter.
The mating MAPK pathway and their output responses strength in S. cerevisiae and C. albicans.