Phenotypic consequences of 1,000 generations of selection at elevated CO2 in a green alga

Estimates of the effect of increasing atmospheric CO2 concentrations on future global plant production rely on the physiological response of individual plants or plant communities when exposed to high CO2 (refs 1-6). Plant populations may adapt to the changing atmosphere, however, such that the evolved plant communities of the next century are likely to be genetically different from contemporary communities. The properties of these future communities are unknown, introducing a bias of unknown sign and magnitude into projections of global carbon pool dynamics. Here we report a long-term selection experiment to investigate the phenotypic consequences of selection for growth at elevated CO2 concentrations. After about 1,000 generations, selection lines of the unicellular green alga Chlamydomonas failed to evolve specific adaptation to a CO2 concentration of 1,050 parts per million. Some lines, however, evolved a syndrome involving high rates of photosynthesis and respiration, combined with higher chlorophyll content and reduced cell size. These lines also grew poorly at ambient concentrations of CO2. We tentatively attribute this outcome to the accumulation of conditionally neutral mutations in genes affecting the carbon concentration mechanism.     

The double helix in clinical practice

The discovery of the double helix half a century ago has so far been slow to affect medical practice, but significant transformations are likely over the next 50 years. Changes to the way medicine is practised and new doctors are trained will be required before potential benefits are realized.     

Interconversion of CD45R subsets of CD4 T cells in vivo

T lymphocytes express multiple forms of the leukocyte common antigen CD45, transcribed by alternative usage of leukocyte-common antigen exons 4-6. Species-specific monoclonal antibodies against restricted epitopes (CD45R) of the antigen subdivide CD4 T cells into reciprocal subsets expressing either the high molecular weight isoforms CD45RA or RB or a molecule in which exons 4-6 have been spliced out (CD45R0). CD45R+ or RB+ CD4 T cells are potent in graft-versus-host reactions, and interleukin-2 related activities, whereas the CD45R0+ subset responds in vitro to recall antigens and provides help for antibody synthesis. It is unclear whether CD45R subsets derive from separate lineages, or are products of unidirectional or reversible differentiation. We show by transferring CD45R+ or CD45R- allotype-marked CD4 T cells into athymic nude rats that both subsets routinely generate cells of the opposite phenotype with a function that follows phenotype, not parentage. The recent equation of CD45R subsets as maturation stages representing 'naive' and 'memory' T cells is difficult to reconcile with this finding.     

Regulation of glucose transporter messenger RNA in insulin-deficient states

Recent studies have indicated that a family of structurally related proteins with distinct but overlapping tissue distributions are responsible for facilitative glucose transport in mammalian tissues. Insulin primarily stimulates glucose transport by inducing the redistribution of a unique glucose transporter protein from an intracellular pool to the plasma membrane. This 509-amino-acid integral membrane protein, termed GLUT-4, is the main insulin-responsive glucose transporter in adipose and muscle tissues. We have observed a dramatic decrease (tenfold) in the steady-state levels of GLUT-4 messenger RNA in adipose tissue from fasted rats or rats made insulin deficient with streptozotocin. Insulin treatment of the streptozotocin-diabetic rats or refeeding the fasted animals causes a rapid recovery of the GLUT-4 mRNA to levels significantly above those observed in untreated control animals. By contrast, the levels of the erythrocyte/HepG2/rat brain-type glucose transporter mRNA remain essentially unchanged under these conditions. These data suggest that the in vivo expression of GLUT-4 mRNA in rat adipose tissue is regulated by insulin.     

Failure of ascorbic acid to influence brain catecholamines in the guinea-pig

Summary Lack of dietary ascorbic acid lowered plasma levels of ascorbic acid but failed to change levels of brain norepinephrine or dopamine.Investigators adhered during the research described in this report to the policy set forth in the Guide for the Care and Use of Laboratory Animals by the Committee on Revision of the Guide for Laboratory Animal Resources, National Research Council.The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.     

Is the renal vasodilatation induced byβ-adrenoceptor stimulants in the dog mediated through dopamine receptor?

Summary In chloralose-anaesthetized dogs the renal vasodilator effect of isoprenaline is depressed by blockade of either dopamine or -adrenoceptors but the renal vasodilator effect of dopamine is depressed only by blockade of dopamine receptors. This suggests that the vasodilatation induced by -stimulants within the canine kidney is due in part to activation of dopamine receptors.This study was supported by the Life Insurance Medical Research Fund of Australia and New Zealand and by the Australian Kidney Foundation.We thank Mr S. Marshall for technical assistance.     

A family of related ATP-binding subunits coupled to many distinct biological processes in bacteria

Many biological processes are coupled to ATP hydrolysis. We describe here a class of closely related ATP-binding proteins, from several bacterial species, which are associated with a variety of cellular functions including membrane transport, cell division, nodulation in Rhizobium and haemolysin export. These proteins comprise a family of structurally and functionally related subunits which share a common evolutionary origin, bind ATP and probably serve to couple ATP hydrolysis to each of these biological processes. This finding suggests a specific role for ATP in cell division, nodulation during nitrogen fixation and protein export, and allows us to assign a probable function to one of the protein components from each of these systems.     

Sea urchin embryo as a model for analysis of the signaling pathways linking DNA damage checkpoint,DNA repair and apoptosis

DNA integrity checkpoint control was studied in the sea urchin early embryo. Treatment of the embryos with genotoxic agents such as methyl methanesulfonate (MMS) or bleomycin induced the activation of a cell cycle checkpoint as evidenced by the occurrence of a delay or an arrest in the division of the embryos and an inhibition of CDK1/cyclin B activating dephosphorylation. The genotoxic treatment was shown to induce DNA damage that depended on the genotoxic concentration and was correlated with the observed cell cycle delay. At low genotoxic concentrations, embryos were able to repair the DNA damage and recover from checkpoint arrest, whereas at high doses they underwent morphological and biochemical changes characteristic of apoptosis. Finally, extracts prepared from embryos were found to be capable of supporting DNA repair in vitro upon incubation with oligonucleotides mimicking damage. Taken together, our results demonstrate that sea urchin early embryos contain fully functional and activatable DNA damage checkpoints. Sea urchin embryos are discussed as a promising model to study the signaling pathways of cell cycle checkpoint, DNA repair and apoptosis, which upon deregulation play a significant role in the origin of cancer. Received 10 April 2007; accepted 23 April 2007     

A RING-type ubiquitin ligase family member required to repress follicular helper T cells and autoimmunity

Despite the sequencing of the human and mouse genomes, few genetic mechanisms for protecting against autoimmune disease are currently known. Here we systematically screen the mouse genome for autoimmune regulators to isolate a mouse strain, sanroque, with severe autoimmune disease resulting from a single recessive defect in a previously unknown mechanism for repressing antibody responses to self. The sanroque mutation acts within mature T cells to cause formation of excessive numbers of follicular helper T cells and germinal centres. The mutation disrupts a repressor of ICOS, an essential co-stimulatory receptor for follicular T cells, and results in excessive production of the cytokine interleukin-21. sanroque mice fail to repress diabetes-causing T cells, and develop high titres of autoantibodies and a pattern of pathology consistent with lupus. The causative mutation is in a gene of previously unknown function, roquin (Rc3h1), which encodes a highly conserved member of the RING-type ubiquitin ligase protein family. The Roquin protein is distinguished by the presence of a CCCH zinc-finger found in RNA-binding proteins, and localization to cytosolic RNA granules implicated in regulating messenger RNA translation and stability.