Abstract
Author SummarySignal transduction pathways regulate the response of cells to changes in the extracellular environment. Here, we report the identification of Tec1 as the single effector transcription factor of the pheromone response pathway of the human pathogen Candida albicans white cell type. This newly evolved pathway provides us with a unique opportunity to investigate signal transduction pathway evolution. In the C. albicans white-opaque transition, mating-competent opaque cells release mating pheromone that induces mating-incompetent white cells to form a biofilm which facilitates mating of the former. Each of the three major portions of the pathway that regulates white cell pheromone response appears to be derived from an ancestral pathway that is still intact and functional in C. albicans. The upstream portion—including the pheromone, its receptor, trimeric G protein complex, and a MAP kinase cascade—appears to be derived from the mating response pathway; transcription factor Tec1 from the filamentation pathway; and Tec1 target genes from the biofilm biosynthesis pathway. We posit that the sharing of upstream signaling components coordinates white and opaque cell pheromone responses, yet the divergence of downstream pathway components allows each cell type to elicit a unique phenotypic outcome. The white cell pheromone response pathway therefore provides a paradigm for how other such pathways may have evolved.
Highlights
There are numerous examples of how signal transduction pathways within an organism selectively share components [1,2,3,4,5]
We report the identification of Tec1 as the single effector transcription factor of the pheromone response pathway of the human pathogen Candida albicans white cell type
Each of the three major portions of the pathway that regulates white cell pheromone response appears to be derived from an ancestral pathway that is still intact and functional in C. albicans
Summary
There are numerous examples of how signal transduction pathways within an organism selectively share components [1,2,3,4,5]. In the yeast Saccharomyces cerevisiae, components are shared to varying degrees among pathways regulating mating, filamentation, cell wall integrity, ascospore formation, and osmoregulation [6,7,8,9,10] Such examples have not engendered a discussion of how signal transduction pathways evolve. This latter requirement appears to be unique to C. albicans and the highly related species Candida dubliniensis [16] The reason for this dependency may be due in part to a unique signaling system that evolved between opaque and white cells that leads to the formation of a biofilm that can facilitate mating between minority opaque cells [17,18]. White cell biofilms have been shown in vitro to facilitate chemotropism between minority opaque cells of opposite mating types [17], leading to the hypothesis that the white-opaque switching system evolved from the direct ancestor of C .albicans and C. dubliniensis to facilitate mating [18]
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