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- Badeck, FW, et al.
(författare)
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Tree species composition in European pristine forests
- 2001
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Ingår i: Climatic Change. - 0165-0009. ; 51:3-4, s. 307-347
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Tidskriftsartikel (refereegranskat)abstract
- The degree of general applicability across Europe currently achieved with several forest succession models is assessed, data needs and steps for further model development are identified and the role physiology based models can play in this process is evaluated. To this end, six forest succession models (DISCFORM, ForClim, FORSKA-M, GUESS, PICUS v1.2, SIERRA) are applied to simulate stand structure and species composition at 5 European pristine forest sites in different climatic regions. The models are initialized with site-specific soil information and driven with climate data from nearby weather stations. Predicted species composition and stand structure are compared to inventory data. Similarity and dissimilarity in the model results under current climatic conditions as well as the predicted responses to six climate change scenarios are discussed. All models produce good results in the prediction of the right tree functional types. In about half the cases, the dominating species are predicted correctly under the current climate. Where deviations occur, they often represent a shift of the species spectrum towards more drought tolerant species. Results for climate change scenarios indicate temperature driven changes in the alpine elevational vegetation belts at humid sites and a high sensitivity of forest composition and biomass of boreal and temperate deciduous forests to changes in precipitation as mediated by summer drought. Restricted generality of the models is found insofar as models originally developed for alpine conditions clearly perform better at alpine sites than at boreal sites, and vice versa. We conclude that both the models and the input data need to be improved before the models can be used for a robust evaluation of forest dynamics under climate change scenarios across Europe. Recommendations for model improvements, further model testing and the use of physiology based succession models are made.
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- Kuehn, Clemens, et al.
(författare)
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Exploring the impact of osmoadaptation on glycolysis using time-varying response-coefficients
- 2008
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Ingår i: Genome informatics. International Conference on Genome Informatics. - 0919-9454. ; 20, s. 77-90
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Konferensbidrag (refereegranskat)abstract
- We present a model of osmoadaptation in S.cerevisiae based on existing experimental and theoretical work. In order to investigate the impact of osmoadaptation on glycolysis, this model focuses on the interactions between glycolysis and osmoadaptation, namely the production of glycerol and its influence on flux towards pyruvate. Evaluation of this model shows that, depending on initial relations between glycerol and pyruvate production, the increased glycerol production can have a substantial negative effect on the pyruvate production rate. Existing experimental data and a detailed analysis of the model lead to the suggestion of an interaction between activated Hog1 and activators of glycolysis such as Pfk26.
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- Petelenz-Kurdziel, Elzbieta, et al.
(författare)
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Quantitative Analysis of Glycerol Accumulation, Glycolysis and Growth under Hyper Osmotic Stress
- 2013
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Ingår i: PLoS Computational Biology. - : Public Library of Science (PLoS). - 1553-734X .- 1553-7358. ; 9:6
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Tidskriftsartikel (refereegranskat)abstract
- We provide an integrated dynamic view on a eukaryotic osmolyte system, linking signaling with regulation of gene expression, metabolic control and growth. Adaptation to osmotic changes enables cells to adjust cellular activity and turgor pressure to an altered environment. The yeast Saccharomyces cerevisiae adapts to hyperosmotic stress by activating the HOG signaling cascade, which controls glycerol accumulation. The Hog1 kinase stimulates transcription of genes encoding enzymes required for glycerol production (Gpd1, Gpp2) and glycerol import (Stl1) and activates a regulatory enzyme in glycolysis (Pfk26/27). In addition, glycerol outflow is prevented by closure of the Fps1 glycerol facilitator. In order to better understand the contributions to glycerol accumulation of these different mechanisms and how redox and energy metabolism as well as biomass production are maintained under such conditions we collected an extensive dataset. Over a period of 180 min after hyperosmotic shock we monitored in wild type and different mutant cells the concentrations of key metabolites and proteins relevant for osmoadaptation. The dataset was used to parameterize an ODE model that reproduces the generated data very well. A detailed computational analysis using time-dependent response coefficients showed that Pfk26/27 contributes to rerouting glycolytic flux towards lower glycolysis. The transient growth arrest following hyperosmotic shock further adds to redirecting almost all glycolytic flux from biomass towards glycerol production. Osmoadaptation is robust to loss of individual adaptation pathways because of the existence and upregulation of alternative routes of glycerol accumulation. For instance, the Stl1 glycerol importer contributes to glycerol accumulation in a mutant with diminished glycerol production capacity. In addition, our observations suggest a role for trehalose accumulation in osmoadaptation and that Hog1 probably directly contributes to the regulation of the Fps1 glycerol facilitator. Taken together, we elucidated how different metabolic adaptation mechanisms cooperate and provide hypotheses for further experimental studies.
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- Talemi, Soheil Rastgou, et al.
(författare)
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Mathematical modelling of arsenic transport, distribution and detoxification processes in yeast.
- 2014
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Ingår i: Molecular Microbiology. - : Wiley. - 0950-382X .- 1365-2958. ; 92:6, s. 1343-56
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Tidskriftsartikel (refereegranskat)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 modelling 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.
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