Increased phosphorylation of ribosomal protein S6 following microinjection of insulin receptor-kinase into Xenopus oocytes

The protein products of several transforming retroviruses as well as the receptors for several hormones and growth factors, including insulin, have been shown to possess a protein kinase activity in vitro specific for tyrosine residues in protein substrates, including themselves. In the case of pp60src and the insulin receptor, autophosphorylation activates the tyrosine kinase activity towards exogenous substrates. Experiments indicate that, in vivo, many of these viruses or growth factors induce an increase in cellular phosphotyrosine, as well as an increase in the phosphorylation of serine residues on proteins, including ribosomal protein S6. It seems likely that some of the effects of insulin might be mediated by phosphorylation of intracellular substrates by its receptor. As the beta subunit of the receptor is a transmembrane protein, such phosphorylation could occur either while the receptor is still in the membrane or after its internalization. In various cell systems, internalized receptors are degraded, reshuttled back to the plasmalemma or maintained in a separate compartment before reinsertion in the membrane; shuttling of the insulin receptor could provide the opportunity for it to phosphorylate various intracellular components as part of its mechanism of signal transduction. To approach directly the question of whether the receptor can elicit a signal while acting at an intracellular location, we have microinjected Xenopus oocytes with the insulin receptor kinase. The results indicate that an S6 protein-serine kinase is stimulated or an S6 protein-serine phosphatase inhibited by the activity of the insulin receptor, supporting the concept that the insulin receptor acting within the cell can elicit a biological response.     

Fire as the dominant driver of central Canadian boreal forest carbon balance

Changes in climate, atmospheric carbon dioxide concentration and fire regimes have been occurring for decades in the global boreal forest, with future climate change likely to increase fire frequency--the primary disturbance agent in most boreal forests. Previous attempts to assess quantitatively the effect of changing environmental conditions on the net boreal forest carbon balance have not taken into account the competition between different vegetation types on a large scale. Here we use a process model with three competing vascular and non-vascular vegetation types to examine the effects of climate, carbon dioxide concentrations and fire disturbance on net biome production, net primary production and vegetation dominance in 100 Mha of Canadian boreal forest. We find that the carbon balance of this region was driven by changes in fire disturbance from 1948 to 2005. Climate changes affected the variability, but not the mean, of the landscape carbon balance, with precipitation exerting a more significant effect than temperature. We show that more frequent and larger fires in the late twentieth century resulted in deciduous trees and mosses increasing production at the expense of coniferous trees. Our model did not however exhibit the increases in total forest net primary production that have been inferred from satellite data. We find that poor soil drainage decreased the variability of the landscape carbon balance, which suggests that increased climate and hydrological changes have the potential to affect disproportionately the carbon dynamics of these areas. Overall, we conclude that direct ecophysiological changes resulting from global climate change have not yet been felt in this large boreal region. Variations in the landscape carbon balance and vegetation dominance have so far been driven largely by increases in fire frequency.