Desiccation tolerance, the ability for an organism to resume normal metabolism after nearly complete dehydration, has been studied for decades. Nevertheless, its mechanisms and regulation are poorly understood. Correlations between desiccation tolerance and several effectors or regulators of stress pathways have been reported in many species but their physiological significance has not been established in vivo. In this thesis, the yeast Saccharomyces cerevisiae is developed as a model organism for investigating desiccation tolerance. Characterization of wild-type yeast reveals that only one in a million yeast cells growing logarithmically at low cell density survive desiccation, while 20% to 40% of cells from a saturated culture survive. Mutants defective in trehalose biosynthesis, hydrophilins, responses to hyperosmolarity and hypersalinity, ROS scavenging and DNA damage repair are still able to acquire wild-type or near wild-type levels of desiccation tolerance, suggesting that this trait involves a unique constellation of stress factors. A genome-wide screen for mutants that render stationary cells as sensitive as log phase cells identifies only mutations that block respiration. Respiration as a prerequisite for the acquisition of desiccation tolerance is corroborated by respiration inhibitors and by growth on non-fermentable carbon sources. Suppressors that bypass the respiration requirement for desiccation tolerance are isolated and reveal two pathways. One is regulated by the Mediator transcription complex and is associated with the shift from fermentative to respiratory metabolism, while the other is regulated by Ras2p, which participates in many pathways, including responses to changes in nutrient profile and in some stress responses. Further study of these regulators and their targets should provide important clues to the sensors and effectors of desiccation tolerance.
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