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Water is essential to all life on earth. It is a major component that makes up living organisms and plays a vital role in multiple biological processes. It provides a medium for chemical and enzymatic reactions in the cell and is a major player in osmoregulation and the maintenance of cell turgidity. Despite this, many organisms, called anhydrobiotes, are capable of surviving under extremely dehydrated conditions. Less is known about how anhydrobiotes adapt and survive under desiccation stress. Studies have shown that morphological and physiological changes occur in anhydrobiotes in response to desiccation stress. Certain disaccharides and proteins, including heat shock proteins, intrinsically disordered proteins, and hydrophilins, play important roles in the desiccation tolerance of anhydrobiotes. In this review, we summarize the recent findings of desiccation tolerance in the budding yeast Saccharomyces cerevisiae. We also propose that the yeast under desiccation could be used as a model to study neurodegenerative disorders. [ABSTRACT FROM AUTHOR]

Abstract: Here we report that budding yeast mitochondrial DNA protects against salt stress-induced apoptosis. Yeast cells lacking mitochondrial DNA (ρ0) are hypersensitive to salt stress-induced apoptosis, which is mediated by mitochondrial cytochrome c release. In addition, cytochrome c expression is downregulated upon salt stress, suggesting a transcriptionally regulated, homeostatic protection mechanism. The repression of cytochrome c transcription is mediated by transcription factor Mig1. Consistently, deletion of MIG1 induces cytochrome C transcription and yields ρ0 cells that are more sensitive to salt stress. In summary, deletion of mitochondrial function leads to salt stress-induced transcriptional deregulation of cytochrome C, causing apoptosis in yeast. [Copyright &y& Elsevier]

Budding yeast PDS5 is an essential gene in mitosis and is required for chromosome condensation and sister chromatid cohesion. Here we report that PDS also is required in meiosis. Pds5p localizes on chromosomes at all stages during meiotic cycle, except anaphase I. PDS5 plays an important role at first meiotic prophase. Failure in function of PDS5 causes premature separation of chromosomes. The loading of Pds5p onto chromosome requires the function of REC8, but the association of Rec8p with chromosome is independent of PDS5. Mutant analysis and live cell imaging indicate that PDS5 play a role in meiosis II as well. [ABSTRACT FROM AUTHOR]

Background: Anhydrobiotes, such as the yeast Saccharomyces cerevisiae, are capable of surviving almost total loss of water. Desiccation tolerance requires an interplay of multiple events, including preserving the protein function and membrane integrity, preventing and mitigating oxidative stress, maintaining certain level of energy required for cellular activities in the desiccated state. Many of these crucial processes can be controlled and modulated at the level of organelle morphology and dynamics. However, little is understood about what organelle perturbations manifest in desiccation-sensitive cells as a consequence of drying or how this differs from organelle biology in desiccation-tolerant organisms undergoing anhydrobiosis. Results: In this study, electron and optical microscopy was used to examine the dynamic changes of yeast cells during the desiccation process. Dramatic structural changes were observed during the desiccation process, including the diminishing of vacuoles, decrease of lipid droplets, decrease in mitochondrial cristae and increase of ER membrane, which is likely caused by ER stress and unfolded protein response. The survival rate was significantly decreased in mutants that are defective in lipid droplet biosynthesis, or cells treated with cerulenin, an inhibitor of fatty acid synthesis. Conclusion: Our study suggests that the metabolism of lipid droplets and membrane may play an important role in yeast desiccation tolerance by providing cells with energy and possibly metabolic water. Additionally, the decrease in mitochondrial cristae coupled with a decrease in lipid droplets is indicative of a cellular response to reduce the production of reactive oxygen species. [ABSTRACT FROM AUTHOR]

Highlights: [•] Alpha-synuclein binds to lipid droplets in wild-type yeast cells. [•] Alpha-synuclein does not bind to lipid droplets in peroxisome-deficient (pex3Δ) cells. [•] A peroxisome deficiency alters the composition of lipid droplets; acyl chains shorten. [•] The shortened acyl chains contribute to the reduced binding of alpha-synuclein. [ABSTRACT FROM AUTHOR]