Precipitation regime controls bryosphere carbon cycling similarly across contrasting ecosystems

In arctic and boreal ecosystems, ground bryophytes play an important role in regulating carbon (C) exchange between vast belowground C stores and the atmosphere. Climate is changing particularly fast in these high-latitude regions, but it is unclear how altered precipitation regimes will affect C dynamics in the bryosphere (i.e. the ground moss layer including senesced moss, litter and associated biota) and the closely associated upper humus layer, and how these effects will vary across contrasting environmental conditions. Here, we set up a greenhouse experiment in which mesocosms were assembled containing samples of the bryosphere, dominated by the feather moss Hylocomium splendens, and the upper humus layer, that were collected from across a boreal forest chronosequence in northern Sweden which varies strongly in nutrient availability, productivity and soil biota. We tested the effect of variation in precipitation volume and frequency on CO₂ exchange and dissolved organic carbon (DOC) export, and on moss growth. As expected, reduced precipitation volume and frequency lowered net CO₂ efflux, DOC export and moss growth. However, by regulating moisture, the lower bryosphere and humus layers often mediated how precipitation volume and frequency interacted to drive C dynamics. For example, less frequent precipitation reduced moss growth only when precipitation volume was low. When volume was high, high moisture content of the humus layer helped avoid moss desiccation. Variation in precipitation regime affected C cycling consistently in samples collected across the chronosequence, despite large environmental variation along the sequence. This suggests that the bryosphere exerts a strong buffering effect on environmental variation at the forest floor, which leads to similar responses of C cycling to external perturbations across highly contrasting ecosystems. As such, our study indicates that projected increases in droughts and ground evapotranspiration in high-latitude regions resulting from climate change will consistently reduce C losses from moss-dominated ecosystems.     

Physiological and molecular diversity of feather moss associative N2-fixing cyanobacteria

Cyanobacteria colonizing the feather moss Pleurozium schreberi were isolated from moss samples collected in northern Sweden and subjected to physiological and molecular characterization. Morphological studies of isolated and moss-associated cyanobacteria were carried out by light microscopy. Molecular tools were used for cyanobacteria identification, and a reconstitution experiment of the association between non-associative mosses and cyanobacteria was conducted. The influence of temperature on N2 fixation in the different cyanobacterial isolates and the influence of light and temperature on N2-fixation rates in the moss were studied using the acetylene reduction assay. Two different cyanobacteria were effectively isolated from P. schreberi: Nostoc sp. and Calothrix sp. A third genus, Stigonema sp. was identified by microscopy, but could not be isolated. The Nostoc sp. was found to fix N2 at lower temperatures than Calothrix sp. Nostoc sp. and Stigonema sp. were the predominant cyanobacteria colonizing the moss. The attempt to reconstitute the association between the moss and cyanobacteria was successful. The two isolated genera of cyanobacteria in feather moss samples collected in northern Sweden differ in their temperature optima, which may have important ecological implications.     

The effect of altered macroclimate on N-fixation by boreal feather mosses

Plant productivity is predicted to increase in boreal forests owing to climate change, but this may depend on whether N inputs from biological N-fixation also increases. We evaluated how alteration of climatic factors affects N input from a widespread boreal N-fixer, i.e. cyanobacteria associated with the feather moss Pleurozium schreberi. In each of 10 forest stands in northern Sweden, we established climate-change plots, including a control (ambient climate) plot and three plots experiencing a +2°C temperature increase, an approximately threefold reduction in precipitation frequency, and either 0.07, 0.29 or 1.16 times normal summer precipitation. We monitored N-fixation in these plots five times between 2007 and 2009, and three times in 2010 after climate treatments ended to assess their recovery. Warmer temperatures combined with less frequent precipitation reduced feather moss moisture content and N-fixation rates regardless of total precipitation. After climate treatments ended, recovery of N-fixation rates occurred on the scale of weeks to months, suggesting resilience of N-fixation to changes in climatic conditions. These results suggest that modelling of biological N-inputs in boreal forests should emphasize precipitation frequency and evaporative water loss in conjunction with elevated temperature rather than absolute changes in mean precipitation.     

The down-regulation of the mitogenic fibrinogen receptor (MFR) in serum-containing medium does not occur in defined medium

Normal human hemopoietic cells such as early bone marrow progenitors, or lymphoma-derived cell lines such as Raji or JM cells, possess a low-affinity receptor specific for fibrinogen. This receptor triggers a mitogenic effect. It differs from the glycoprotein IIb-IIIa which is involved in fibrinogen-induced platelet aggregation. We demonstrate here that this mitogenic fibrinogen receptor (MFR) can be internalized or reexpressed, depending on culture conditions. Internalization was temperature-dependent. At 37 degrees C in the presence of cycloheximide or actinomycin D, the half-life of cell surface MFRs was 2 h, independent of receptor occupancy. Binding of fibrinogen to the MFR resulted in a down-regulation which was fibrinogen dose-dependent. This occurred in serum-supplemented medium but not in defined medium supplemented with fatty acids. Reexpression of MFRs could be induced in 28 to 42 h by serum removal. The down-regulation of mitogenic receptors in plasma or serum could explain why normal cells do not proliferate in the peripheral blood.     

Variation in the effectiveness of biotic defence: the case of an opportunistic ant-plant protection mutualism

Benefits to plants in facultative ant protection mutualisms are highly variable. This allows examination of the sources of this variation and the mechanisms by which ants protect plants. We studied opportunistic interactions between ants and an extrafloral nectary-bearing vine, Dioscorea praehensilis, during 3 different years. Variation in plant protection among years was striking. Several factors affected the effectiveness of the biotic defence. Stems recently emerged from the underground tuber were self-supporting, contacting no other plants and encountering few foraging ants. Stems then became lianescent, and contact with supporting plants greatly increased ant recruitment. Both species and number of ant workers influenced the effect of ants on the major herbivore, the chrysomelid beetle Lilioceris latipennis. Protective actions included limitation of oviposition (reduction in the number of eggs laid on the plant) and predation, leading to increased larval mortality. The probability of successful predation was strongly dependent on larval size. If temporarily low ant-patrolling activity allows larvae to grow beyond a critical size, their mechanical (thick integument) or chemical (plant-derived compounds in a fecal shield) defences become more effective against ants. Secondary metabolites derived from the host plant thus appear to be important for the anti-predator mechanisms of this beetle, being necessary for its survival and reproduction on a host plant that actively recruits ants as a biotic defence against herbivores.     

Microbe-plant competition, allelopathy and arctic plants

Michelsen et al. (1995) present results of an experiment in which aqueous leaf extracts of three arctic woody plant species were found to inhibit growth and nutrient acquisition of three graminoid species, and suggested that microbial nutrient immobilisation, rather than allelopathy, was responsible for the observed trends. In doing this they also question previous work proposing that the Arctic dwarf shrub Empetrum hermaphroditum is allelopathic. We suggest that their conclusions are not unequivocally supported by their data. Firstly we indicate that the approaches used for estimating microbial nutrient immobilisation are questionable. Secondly we indicate that most of the trends that they discussed are based on data in which the treatments and controls are not significantly different for the majority of cases. Finally we respond specifically to their criticisms of previous work on E. hermaphroditum. While the question of how arctic plants interact is an interesting one, we conclude that this question cannot be answered by their data. Received: 20 November 1995 /Accepted: 10 July 1996     

7-Ketocholesterol Incorporation into Sphingolipid/Cholesterol-enriched (Lipid Raft) Domains Is Impaired by Vitamin E: A SPECIFIC ROLE FOR ��-TOCOPHEROL WITH CONSEQUENCES ON CELL DEATH*

Cholesterol oxides, in particular 7-ketocholesterol, are proatherogenic compounds that induce cell death in the vascular wall when localized in lipid raft domains of the cell membrane. Deleterious effects of 7-ketocholesterol can be prevented by vitamin E, but the molecular mechanism involved is unclear. In this study, unlike γ-tocopherol, the α-tocopherol vitamin E form was found to prevent 7-ketocholesterol-mediated apoptosis of A7R5 smooth muscle cells. To be operative, α-tocopherol needed to be added to the cells before 7-ketocholesterol, and its anti-apoptotic effect was reduced and even suppressed when added together or after 7-ketocholesterol, respectively. Both pre- and co-treatment of the cells with α-tocopherol resulted in the redistribution of 7-ketocholesterol out of the sphingolipid/cholesterol-enriched (lipid raft) domains. In turn, fewer amounts of α-tocopherol associated with lipid rafts on 7-ketocholesterol-pretreated cells compared with untreated cells, with no prevention of cell death in this case. In further support of the implication of lipid raft domains, the dephosphorylation/inactivation of Akt-PKB was involved in the 7-ketocholesterol-induced apoptosis. Akt-PKB dephosphorylation was prevented by α-tocopherol, but not γ-tocopherol pretreatment.It has been suggested that cholesterol oxide-induced apoptosis is a key event in the initiation and progression of atherosclerosis lesions (1, 2). In the initial step of the disease, cholesterol oxides in modified low density lipoproteins were found to promote the death of endothelial cells lining the intravascular lumen (1, 2). In more advanced stages and as the atherosclerotic lesion progresses, cholesterol oxides could also contribute to the destruction of foam cells and vascular smooth muscle cells, to the formation of the lipid core, to the reduction of cell proliferation, and eventually to plaque destabilization (1, 2). Among cholesterol oxides that are mainly synthesized during oxidation of low density lipoproteins, 7-ketocholesterol is one of the most abundant in plasma and atherosclerotic lesions (3). Moreover, in a number of cell models, it has been established that 7-ketocholesterol is one of the cholesterol oxide derivatives with the highest pro-apoptotic potential (4, 5). The 7-ketocholesterol derivative associates preferentially with membrane lipid raft domains (6), which are characterized by the lateral packing of glycosphingolipids, sphingolipids, and cholesterol. Because of their insolubility in cold non-ionic detergents, rafts are also called detergent-resistant membranes (7). These structures are thought to be involved in cellular signaling mechanisms (8, 9). It is worthy of note that 7-ketocholesterol has been shown to induce cell death through inactivation of the phosphatidylinositol 3-kinase/Akt signaling pathway (10), which is known to be highly specific to lipid raft domains (9).Vitamin E is composed of closely related molecules, i.e. tocopherols and tocotrienols, which are each composed of four α, β, γ, and δ analogues. Although vitamin E was widely studied for its ability to prevent cellular damage by reactive oxygen species, it has recently been the subject of intense research for its putative, non-antioxidant functions (11, 12). Among the various forms of vitamin E, α-tocopherol is most abundant in the body as it is specifically recognized by the liver α-tocopherol transfer protein. Although several studies have shown that vitamin E has the ability to counteract the pro-apoptotic effect of 7-ketocholesterol in cultured cells (10, 13), the underlying molecular mechanism is unclear.In the present study the molecular mechanism involved in the vitamin E-mediated protection against apoptosis induced by 7-ketocholesterol was investigated on the well known A7R5 aortic smooth muscle cell model. It is reported here that α-tocopherol, but not γ-tocopherol, effectively protects the cells against 7-ketocholesterol-induced apoptosis when applied as a pretreatment before the addition of 7-ketocholesterol. Unlike γ-tocopherol, α-tocopherol was able to activate the Akt-PKB anti-apoptotic signaling pathway in the lipid raft domains (14), leading to phosphorylation and, thus, inactivation of Bad (15). Most importantly, the protective effect of α-tocopherol is shown to operate through its prior incorporation into the lipid raft domains of the plasma membrane, which leads to the subsequent exclusion and, thus, inactivation of 7-ketocholesterol.     

Molecular basis of the attenuated phenotype of human APOBEC3B DNA mutator enzyme

The human APOBEC3A and APOBEC3B genes (A3A and A3B) encode DNA mutator enzymes that deaminate cytidine and 5-methylcytidine residues in single-stranded DNA (ssDNA). They are important sources of mutations in many cancer genomes which show a preponderance of CG->TA transitions. Although both enzymes can hypermutate chromosomal DNA in an experimental setting, only A3A can induce double strand DNA breaks, even though the catalytic domains of A3B and A3A differ by only 9% at the protein level. Accordingly we sought the molecular basis underlying A3B attenuation through the generation of A3A-A3B chimeras and mutants. It transpires that the N-terminal domain facilitates A3B activity while a handful of substitutions in the catalytic C-terminal domain impacting ssDNA binding serve to attenuate A3B compared to A3A. Interestingly, functional attenuation is also observed for the rhesus monkey rhA3B enzyme compared to rhA3A indicating that this genotoxic dichotomy has been selected for and maintained for some 38 million years. Expression of all human ssDNA cytidine deaminase genes is absent in mature sperm indicating they contribute to somatic mutation and cancer but not human diversity.