Cell volume is an important parameter for modelling cellular processes. Temperature-induced variability of cellular size, volume, intracellular granularity, a fraction of budding cells of yeast Saccharomyces cerevisiae CEN.PK 113–7D (in anaerobic glucose unlimited batch cultures) were measured by flow cytometry and matched with the performance of the biomass growth (maximal specific growth rate (μ_max), specific rate of glucose consumption, the rate of maintenance, biomass yield on glucose). The critical diameter of single cells was 7.94 μm and it is invariant at growth temperatures above 18.5°C. Below 18.5°C, it exponentially increases up to 10.2 μm. The size of the bud linearly depends on μ_max, and it is between 50% at 5°C and 90% at 31°C of the averaged single cell. The intracellular granularity (side scatter channel (SSC)-index) negatively depends on μ_max. There are two temperature regions (5–31°C vs. 33–40°C) where the relationship between SSC-index and various cellular parameters differ significantly. In supraoptimal temperature range (33–40°C), cells are less granulated perhaps due to a higher rate of the maintenance. There is temperature dependent passage through the checkpoints in the cell cycle which influences the μ_max. The results point to the existence of two different morphological states of yeasts in these different temperature regions.

Temperature has a strong influence on most individual biochemical reactions. Despite this, many organisms have the remarkable ability to keep certain physiological fluxes approximately constant over an extended temperature range. In this study, we show how temperature compensation can be considered as a pathway phenomenon rather than the result of a single‐enzyme property. Using metabolic control analysis, it is possible to identify reaction networks that exhibit temperature compensation. Because most activation enthalpies are positive, temperature compensation of a flux can occur when certain control coefficients are negative. This can be achieved in networks with branching reactions or if the first irreversible reaction is regulated by a feedback loop. Hierarchical control analysis shows that networks that are dynamic through regulated gene expression or signal transduction may offer additional possibilities to bring the apparent activation enthalpies close to zero and lead to temperature compensation. A calorimetric experiment with yeast provides evidence that such a dynamic temperature adaptation can actually occur.

SUMMARY: The aim of this study was to determine the effects of seasonal temperature variation on the functional properties of lactate dehydrogenase (LDH) from white muscle and liver of Norwegian coastal cod (Gadus morhua) and the possible relevance of LDH allelic variability for thermal acclimation. Two groups of fishes were acclimated to 4°C or 12°C for one year. Polymorphism was observed in only one (Ldh-B) of the three Ldh loci expressed in cod liver and/or muscle. Isozyme expression remained unchanged regardless of acclimation temperature(TA). The products of locus Ldh-B comprise only 14–19% (depending on the tissue) of total LDH activities and,consequently, differences between phenotypes are negligible in terms of their effect on LDH total performance. No kinetic(\batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(K_{\mathrm{m}}^{\mathrm{PYR}}\) \end{document}, \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(K_{\mathrm{si}}^{\mathrm{PYR}}\) \end{document}, Vmax) or thermodynamic (Ea,Δ G) differences were found among Ldh-B phenotypes. Clear kinetic differences were observed between LDH isoforms in the two tissues. However, the Arrhenius activation energy (Ea) for pyruvate reduction was the same for both tissues (Ea=47 kJ mol–1) at TA=12°C. Factors TA, tissue and phenotype did not reveal a significant effect on the Gibbs free energy change (ΔG) of the reaction(55.5 kJ mol–1). However, at TA=4°C,the Ea was increased (Ea=53–56 kJ mol–1) and the temperature dependence of the constant of substrate inhibition for pyruvate(\batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(K_{\mathrm{si}}^{\mathrm{PYR}}\) \end{document}) decreased in both muscle and liver.In conclusion, the strategies of LDH adjustment to seasonal temperature variations in cod involve changes in LDH concentration (quantitative),adjustment of thermodynamic (Ea) and kinetic(\batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(K_{\mathrm{si}}^{\mathrm{PYR}}\) \end{document}) properties of the LDH(modulative) but not the expression of alternative isoforms (qualitative). We assume that the observed increase in Ea and the decrease of temperature dependence of \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(K_{\mathrm{si}}^{\mathrm{PYR}}\) \end{document} at low TA is the result of structural changes of the LDH molecule(temperature-driven protein folding). We propose a new mechanism of metabolic compensation of seasonal temperature variations – cold acclimation results in changes in the kinetic and thermodynamic properties of LDH in a way that favours aerobic metabolism through reduction of the competition of LDH for pyruvate in normoxic conditions.