University of Dundee

About: University of Dundee is a education organization based out in Dundee, United Kingdom. It is known for research contribution in the topics: Population & Protein kinase A. The organization has 19258 authors who have published 39640 publications receiving 1919433 citations. The organization is also known as: Universitas Dundensis & Dundee University.

Temperature and algal growth

Abstract: summary Genotypic variation in the temperature optimum for resource-saturated growth of microalgae has been used to provide envelopes of μm (maximum specific growth rate) as a function of temperature. The Q10 value for μm for batch-cultured algae with optimal growth temperatures in the range 5–40°C is 1.88; rather higher values (Q10= 2.08–2.19) are found, albeit with lower μ values at a given temperature, for continuous cultures. The envelope approach selects μ values for the smallest cells from the taxa (members of the Chlorophyta and Bacillariophyta) with the highest μ values at a given temperature. Larger cell size, or membership of the Dinophyta, gives a decreased μ at a given temperature. Phenotypic change in μ, within a given genotype grown at sub-optimal temperatures, has a Q10 in excess of 1.88. Analysis of constraints on the resource-saturated value of μ in the fastest-growing micro-algae suggest that, at their temperature optima, the cells are close (within a factor of 2) to their maximum potential growth rate, based on the known kinetic properties of their catalysts, the need for kinetic heterogenity in catalyses in metabolic pathways, and the need to allocate some cell resources to structural and storage components. Phenotypic and genotypic responses to lower temperatures for growth, in terms of reallocation of resources to increase the quantity per unit biomass of catalyst? as a means of offsetting lower catalytic capacity at lower temperatures, are limited. An exception is the light-harvesting and reaction centre apparatus which catalyses the temperature-insensitive processes of light absorption, excitation energy transfer and primary photochemistry, and which is present (as assayed by photosynthetic pigment per unit biomass) in smaller relative amounts during resource-saturated growth at lower temperatures. The involvement of other low-temperature ‘adaptations’ (e.g. homeoviscous behaviour of thylakoid membranes) in offsetting low temperature effects on catalytic rates is not clear. The scope for increasing the quantity of temperature-sensitive catalysts in the biomass as a means of offsetting the effects of low temperature on resource-saturated μ is potentially higher in the Dinophyta with their relatively low μ at their temperature optimum; however, this option does not appear to be taken up by the Dinophyta which have unexceptional Q10 values for μ. For resource-limited growth, the phenotypic effect of suboptimal temperatures on growth, when light is the limiting resource, is often less marked than when growth is light saturated. When a chemical nutrient is limiting, the temperature effect on growth of a given genotype is often, but not invariably, decreased. Cases in which the effect of temperature on growth rate is decreased under light-limiting conditions can be interpreted in terms of the intrinsically low Q10 of growth when temperature-insensitive reactions (light absorption, excitation energy transfer, primary photochemistry) are limiting and the acclimatory effects of changed temperature and light regimes for growth on resource allocation between pigment-protein complexes and downstream catalysts of temperature-sensitive reactions. Cases in which light-limited growth rate is quite temperature sensitive may be accounted for by a decrease in absorptance as a result of a lower pigment content per cell at low growth temperatures. For growth limited by chemical nutrients, the variable responses make analysis difficult. It is tempting to assign a low Q10 for μ under these conditions to a limitation by some transport process (diffusion through unstirred layers, or, less plausibly, the cell membrane) with a low Q10, although the evidence favouring this interpretation is not abundant.

The p53 tumour suppressor gene

Abstract: Background Abnormalities of the p53 tumour suppressor gene are thought to be central to the development of a high proportion of human tumours. This article reviews current understanding of its function and potential clinical significance. Methods Material was identified from previous review articles, references cited in original papers, a Medline search of the literature over the 12 months to January 1998, and by scanning the latest issues of relevant journals. Results and conclusion p53 is considered to be a stress response gene, its product (the p53 protein) acting to induce cell cycle arrest or apoptosis in response to DNA damage, thereby maintaining genetic stability in the organism. These functions are executed by a complex and incompletely understood series of steps known as the ‘p53 pathway’, part of which involves induction of the expression of a number of other genes. As p53 is the most commonly mutated gene in human cancer, it has attracted a great deal of interest as a prognostic factor, diagnostic tool and therapeutic target. However, despite many promising studies, its potential in practical cancer management has still to be realized. © 1998 British Journal of Surgery Society Ltd

The Antidiabetic Drug Metformin Activates the AMP-Activated Protein Kinase Cascade via an Adenine Nucleotide-Independent Mechanism

Abstract: Metformin, a drug widely used to treat type 2 diabetes, was recently shown to activate the AMP-activated protein kinase (AMPK) in intact cells and in vivo. In this study we addressed the mechanism for this effect. In intact cells, metformin stimulated phosphorylation of the key regulatory site (Thr-172) on the catalytic (alpha) subunit of AMPK. It did not affect phosphorylation of this site by either of two upstream kinases in cell-free assays, although we were able to detect an increase in upstream kinase activity in extracts of metformin-treated cells. Metformin has been reported to be an inhibitor of complex 1 of the respiratory chain, but we present evidence that activation of AMPK in two different cell types is not a consequence of depletion of cellular energy charge via this mechanism. Whereas we have not established the definitive mechanism by which metformin activates AMPK, our results show that the mechanism is different from that of the existing AMPK-activating agent, 5-aminoimidazole-4-carboxamide (AICA) riboside. Metformin therefore represents a useful new tool to study the consequences of AMPK activation in intact cells and in vivo. Our results also show that AMPK can be activated by mechanisms other than changes in the cellular AMP-to-ATP ratio.