The effect of short term exposures to 100% oxygen on the fine structure of proximal convoluted tubules

Résumé Des rats ont été maintenus dans une athmosphère d'oxygène pur sous une pression de 600 mm de mercure durant des périodes de 3 et 7 jours. Les observations faites au microscope électronique sur les tissus prélevés dans le rein ont montré qu'après 7 jours de traitement les mitochondries et les particules de corps gras ont subi dans la cellule d'importantes modifications. Après 3 jours seulement, on n'observait accun changement de l'ultrastructure.     

Voltage-sensing residues in the S4 region of a mammalian K+ channel

The ability of ion-channel proteins to respond to a change of the transmembrane voltage is one of the basic mechanisms underlying electrical excitability of nerve and muscle membranes. The voltage sensor has been postulated to be the fourth putative transmembrane segment (S4) of voltage-activated Na+, Ca2+ and K+ channels. Mutations of positively charged residues within S4 alter gating of Na and Shaker-type K+ channels, but quantitative correlations between the charge or a residue in S4 and the gating valence of the channel have not yet been established. Here, with improved resolution of the voltage dependence of steady-state activation, we present estimates of the equivalent gating valence with sufficient precision to allow quantitative examination of the contribution of individual charged residues to the gating valence of a mammalian non-inactivating K+ channel. We conclude that at least part of the gating charge associated with channel activation is indeed contributed by charged residues within the S4 segment.     

Phosphorylation of the nicotinic acetylcholine receptor regulates its rate of desensitization

Recent studies have provided evidence for a role of protein phosphorylation in the regulation of the function of various potassium and calcium channels (for reviews, see refs 1, 2). As these ion channels have not yet been isolated and characterized, it has not been possible to determine whether phosphorylation of the ion channels themselves alters their properties or whether some indirect mechanism is involved. In contrast, the nicotinic acetylcholine receptor, a neurotransmitter-dependent ion channel, has been extensively characterized biochemically and has been shown to be directly phosphorylated. The phosphorylation of this receptor is catalysed by at least three different protein kinases (cyclic AMP-dependent protein kinase, protein kinase C and a tyrosine-specific protein kinase) on seven different phosphorylation sites. However, the functional significance of phosphorylation of the receptor has been unclear. We have now examined the functional effects of phosphorylation of the nicotinic acetylcholine receptor by cAMP-dependent protein kinase. We investigated the ion transport properties of the purified and reconstituted acetylcholine receptor before and after phosphorylation. We report here that phosphorylation of the nicotinic acetylcholine receptor on the gamma- and delta-subunits by cAMP-dependent protein kinase increases the rate of the rapid desensitization of the receptor, a process by which the receptor is inactivated in the presence of acetylcholine (ACh). These results provide the first direct evidence that phosphorylation of an ion channel protein modulates its function and suggest that phosphorylation of postsynaptic receptors in general may play an important role in synaptic plasticity.     

Genome-wide expression dynamics of a marine virus and host reveal features of co-evolution

Interactions between bacterial hosts and their viruses (phages) lead to reciprocal genome evolution through a dynamic co-evolutionary process. Phage-mediated transfer of host genes--often located in genome islands--has had a major impact on microbial evolution. Furthermore, phage genomes have clearly been shaped by the acquisition of genes from their hosts. Here we investigate whole-genome expression of a host and phage, the marine cyanobacterium Prochlorococcus MED4 and the T7-like cyanophage P-SSP7, during lytic infection, to gain insight into these co-evolutionary processes. Although most of the phage genome was linearly transcribed over the course of infection, four phage-encoded bacterial metabolism genes formed part of the same expression cluster, even though they are physically separated on the genome. These genes--encoding photosystem II D1 (psbA), high-light inducible protein (hli), transaldolase (talC) and ribonucleotide reductase (nrd)--are transcribed together with phage DNA replication genes and seem to make up a functional unit involved in energy and deoxynucleotide production for phage replication in resource-poor oceans. Also unique to this system was the upregulation of numerous genes in the host during infection. These may be host stress response genes and/or genes induced by the phage. Many of these host genes are located in genome islands and have homologues in cyanophage genomes. We hypothesize that phage have evolved to use upregulated host genes, leading to their stable incorporation into phage genomes and their subsequent transfer back to hosts in genome islands. Thus activation of host genes during infection may be directing the co-evolution of gene content in both host and phage genomes.     

Outgassing from Amazonian rivers and wetlands as a large tropical source of atmospheric CO2

Terrestrial ecosystems in the humid tropics play a potentially important but presently ambiguous role in the global carbon cycle. Whereas global estimates of atmospheric CO2 exchange indicate that the tropics are near equilibrium or are a source with respect to carbon, ground-based estimates indicate that the amount of carbon that is being absorbed by mature rainforests is similar to or greater than that being released by tropical deforestation (about 1.6 Gt C yr-1). Estimates of the magnitude of carbon sequestration are uncertain, however, depending on whether they are derived from measurements of gas fluxes above forests or of biomass accumulation in vegetation and soils. It is also possible that methodological errors may overestimate rates of carbon uptake or that other loss processes have yet to be identified. Here we demonstrate that outgassing (evasion) of CO2 from rivers and wetlands of the central Amazon basin constitutes an important carbon loss process, equal to 1.2 +/- 0.3 Mg C ha-1 yr-1. This carbon probably originates from organic matter transported from upland and flooded forests, which is then respired and outgassed downstream. Extrapolated across the entire basin, this flux-at 0.5 Gt C yr-1-is an order of magnitude greater than fluvial export of organic carbon to the ocean. From these findings, we suggest that the overall carbon budget of rainforests, summed across terrestrial and aquatic environments, appears closer to being in balance than would be inferred from studies of uplands alone.