Article

Biophysical properties of Saccharomyces cerevisiae and their relationship with HOG pathway activation.

Theoretical Biophysics, Humboldt University, Invaliden Str 42, 10115 Berlin, Germany.
Biophysics of Structure and Mechanism (Impact Factor: 2.44). 10/2010; 39(11):1547-56. DOI: 10.1007/s00249-010-0612-0
Source: PubMed

ABSTRACT Parameterized models of biophysical and mechanical cell properties are important for predictive mathematical modeling of cellular processes. The concepts of turgor, cell wall elasticity, osmotically active volume, and intracellular osmolarity have been investigated for decades, but a consistent rigorous parameterization of these concepts is lacking. Here, we subjected several data sets of minimum volume measurements in yeast obtained after hyper-osmotic shock to a thermodynamic modeling framework. We estimated parameters for several relevant biophysical cell properties and tested alternative hypotheses about these concepts using a model discrimination approach. In accordance with previous reports, we estimated an average initial turgor of 0.6 ± 0.2 MPa and found that turgor becomes negligible at a relative volume of 93.3 ± 6.3% corresponding to an osmotic shock of 0.4 ± 0.2 Osm/l. At high stress levels (4 Osm/l), plasmolysis may occur. We found that the volumetric elastic modulus, a measure of cell wall elasticity, is 14.3 ± 10.4 MPa. Our model discrimination analysis suggests that other thermodynamic quantities affecting the intracellular water potential, for example the matrix potential, can be neglected under physiological conditions. The parameterized turgor models showed that activation of the osmosensing high osmolarity glycerol (HOG) signaling pathway correlates with turgor loss in a 1:1 relationship. This finding suggests that mechanical properties of the membrane trigger HOG pathway activation, which can be represented and quantitatively modeled by turgor.

0 Bookmarks
 · 
143 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Arsenic has a dual role as causative and curative agent of human disease. Therefore, there is considerable interest in elucidating arsenic toxicity and detoxification mechanisms. By an ensemble modeling approach, we identified a best parsimonious mathematical model which recapitulates and predicts intracellular arsenic dynamics for different conditions and mutants, thereby providing novel insights into arsenic toxicity and detoxification mechanisms in yeast, which could partly be confirmed experimentally by dedicated experiments. Specifically, our analyses suggest that: i) arsenic is mainly protein-bound during short-term (acute) exposure, whereas glutathione-conjugated arsenic dominates during long-term (chronic) exposure; ii) arsenic is not stably retained, but can leave the vacuole via an export mechanism; and iii) Fps1 is controlled by Hog1-dependent and Hog1-independent mechanisms during arsenite stress. Our results challenge glutathione depletion as a key mechanism for arsenic toxicity and instead suggest that iv) increased glutathione biosynthesis protects the proteome against the damaging effects of arsenic and that v) widespread protein inactivation contributes to the toxicity of this metalloid. Our work in yeast may prove useful to elucidate similar mechanisms in higher eukaryotes and have implications for the use of arsenic in medical therapy.
    Molecular Microbiology 05/2014; · 5.03 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Yeast cells are well adapted to interfacial habitats, such as the surfaces of soil or plants, where they can resist frequent fluctuations between wet and dry conditions. Saccharomyces cerevisiae is recognized as an anhydrobiotic organism, and it has been the subject of numerous studies that aimed to elucidate this ability. Extensive data have been obtained from these studies based on a wide range of experimental approaches, which have added significantly to our understanding of the cellular bases and mechanisms of resistance to desiccation. The aim of this review is to provide an integrated view of these mechanisms in yeast and to describe the survival kit of S. cerevisiae for anhydrobiosis. This kit comprises constitutive and inducible mechanisms that prevent cell damage during dehydration and rehydration. This review also aims to characterize clearly the phenomenon of anhydrobiosis itself based on detailed descriptions of the causes and effects of the constraints imposed on cells by desiccation. These constraints mainly lead to mechanical, structural, and oxidative damage to cell components. Considerations of these constraints and the possible utilization of components of the survival kit could help to improve the survival of sensitive cells of interest during desiccation.
    Applied Microbiology and Biotechnology 08/2014; · 3.81 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Yeast and other walled cells possess high internal turgor pressure that allows them to grow and survive in the environment. This turgor pressure however may oppose the invagination of the plasma membrane needed for endocytosis. Here, we study the effects of turgor pressure on endocytosis in the fission yeast Schizosaccharomyces pombe by time lapse imaging of individual endocytic sites. Decreasing effective turgor pressure by addition of sorbitol to the media significantly accelerates early steps in the endocytic process prior to actin assembly and membrane ingression, but does not affect the velocity or depth of ingression of the endocytic pit in wildtype cells. Sorbitol also rescues endocytic ingression defects of certain endocytic mutants and of cells treated with a low dose of the actin inhibitor Latrunculin A. Endocytosis proceeds after removal of the cell wall, suggesting that the cell wall does not contribute mechanically to this process. These studies suggest that endocytosis is governed by a mechanical balance between local actin-dependent inward forces and opposing forces from high internal turgor pressure on the plasma membrane.
    Molecular biology of the cell 01/2014; · 5.98 Impact Factor

Full-text (3 Sources)

Download
56 Downloads
Available from
May 15, 2014