Scale-dependent bi-trophic interactions in a semi-arid savanna: how herbivores eliminate benefits of nutrient patchiness to plants

The scale of resource heterogeneity may influence how resources are locally partitioned between co-existing large and small organisms such as trees and grasses in savannas. Scale-related plant responses may, in turn, influence herbivore use of the vegetation. To examine these scale-dependent bi-trophic interactions, we varied fertilizer [(nitrogen (N)/phosphorus (P)/potassium (K)] applications to patches to create different scales of nutrient patchiness (patch size 2 × 2 m, 10 × 10 m, or whole-plot 50 × 50 m) in a large field experiment in intact African savanna. Within-patch fertilizer concentration and the total fertilizer load per plot were independently varied. We found that fertilization increased the leaf N and P concentrations of trees and grasses, resulting in elevated utilization by browsers and grazers. Herbivory off-take was particularly considerable at higher nutrient concentrations. Scale-dependent effects were weak. The net effect of fertilization and herbivory was that plants in fertilized areas tended to grow less and develop smaller rather than larger standing biomass compared to plants growing in areas that remained unfertilized. When all of these effects were considered together at the community (plot) level, herbivory completely eliminated the positive effects of fertilization on the plant community. While this was true for all scales of fertilization, grasses tended to profit more from coarse-grained fertilization and trees from fine-grained fertilization. We conclude that in herbivore-dominated communities, such as the African savanna, nutrient patchiness results in the herbivore community profiting rather more than the plant community, irrespective of the scale of patchiness. At the community level, the allometric scaling theory’s prediction of plant—and probably also animal—production does not hold or may even be reversed as a result of complex bi-trophic interactions.     

The Ebola virus VP35 protein is a suppressor of RNA silencing

RNA silencing or interference (RNAi) is a gene regulation mechanism in eukaryotes that controls cell differentiation and developmental processes via expression of microRNAs. RNAi also serves as an innate antiviral defence response in plants, nematodes, and insects. This antiviral response is triggered by virus-specific double-stranded RNA molecules (dsRNAs) that are produced during infection. To overcome antiviral RNAi responses, many plant and insect viruses encode RNA silencing suppressors (RSSs) that enable them to replicate at higher titers. Recently, several human viruses were shown to encode RSSs, suggesting that RNAi also serves as an innate defence response in mammals. Here, we demonstrate that the Ebola virus VP35 protein is a suppressor of RNAi in mammalian cells and that its RSS activity is functionally equivalent to that of the HIV-1 Tat protein. We show that VP35 can replace HIV-1 Tat and thereby support the replication of a Tat-minus HIV-1 variant. The VP35 dsRNA-binding domain is required for this RSS activity. Vaccinia virus E3L protein and influenza A virus NS1 protein are also capable of replacing the HIV-1 Tat RSS function. These findings support the hypothesis that RNAi is part of the innate antiviral response in mammalian cells. Moreover, the results indicate that RSSs play a critical role in mammalian virus replication.     

Greater replication and differentiation of preadipocytes in inherited corticosteroid-binding globulin deficiency

Glucocorticoids are pivotal for adipose tissue development. Rodent studies suggest that corticosteroid-binding globulin (CBG) modulates glucocorticoid action in adipose tissue. In humans, both genetic CBG deficiency and suppressed CBG concentrations in hyperinsulinemic states are associated with obesity. We hypothesized that CBG deficiency in humans modulates the response of human preadipocytes to glucocorticoids, predisposing them to obesity. We compared normal preadipocytes with subcultured preadipocytes from an individual with the first ever described complete deficiency of CBG due to a homozygous null mutation. CBG-negative preadipocytes proliferated more rapidly and showed greater peroxisome proliferator-activated receptor-gamma-mediated differentiation than normal preadipocytes. CBG was not expressed in normal human preadipocytes. Glucocorticoid receptor number and binding characteristics and 11beta-hydroxysteroid dehydrogenase activity were similar for CBG-negative and normal preadipocytes. We propose that the increased proliferation and enhanced differentiation of CBG-negative preadipocytes may promote adipose tissue deposition and explain the obesity seen in individuals with genetic CBG deficiency. Furthermore, these observations may be relevant to obesity occurring with suppressed CBG concentrations associated with hyperinsulinemia.     

Modulation by phytochrome of the blue light-induced extracellular acidification by leaf epidermal cells of pea (Pisum sativum l.): a kinetic analysis

Blue light induces extracellular acidification, a prerequisite of cell expansion, in epidermis cells of young pea leaves, by stimulation of the proton pumping-ATPase activity in the plasma membrane. A transient acidification, reaching a maximum 2.5-5 min after the start of the pulse, could be induced by pulses as short as 30 msec. A pulse of more than 3000 micromol m-2 saturated this response. Responsiveness to a second light pulse was recovered with a time constant of about 7 min. The fluence rate-dependent lag time and sigmoidal increase of the acidification suggested the involvement of several reactions between light perception and activation of the ATPase. In wild-type pea plants, the fluence response relation for short light pulses was biphasic, with a component that saturates at low fluence and one that saturates at high fluence. The phytochrome-deficient mutant pcd2 showed a selective loss of the high-fluence component, suggesting that the high-fluence component is phytochrome-dependent and the low-fluence component is phytochrome-independent. Treatment with the calmodulin inhibitor W7 also led to the elimination of the phytochrome-dependent high-fluence component. Simple models adapted from the one used to simulate blue light-induced guard cell opening failed to explain one or more elements of the experimental data. The hypothesis that phytochrome and a blue light receptor interact in a short-term photoresponse is endorsed by model calculations based upon a three-step signal transduction cascade, of which one component can be modulated by phytochrome.     

The membrane potential of Arabidopsis thaliana guard cells; depolarizations induced by apoplastic acidification

The apoplastic pH of guard cells probably acidifies in response to light, since light induces proton extrusion by both guard cells and epidermal leaf cells. From the data presented here, it is concluded that these apoplastic pH changes will affect K⁺ fluxes in guard cells of Arabidopsis thaliana (L.) Heynh. Guard cells of this species were impaled with double-barrelled microelectrodes, to measure the membrane potential (E_m) and the plasma-membrane conductance. Guard cells were found to exhibit two states with respect to their E_m, a depolarized and a hyperpolarized state. Apoplastic acidification depolarized E_m in both states, though the origin of the depolarization differed for each state. In the depolarized state, the change in E_m was the result of a combined pH effect on instantaneously activating conductances and on the slow outward rectifying K⁺ channel (s-ORC). At a more acidic apoplastic pH, the current through instantaneously activated conductances became more inwardly directed, while the maximum conductance of s-ORC decreased. The effect on s-ORC was accompanied by an acceleration of activation and deactivation of the channel. Experiments with acid loading of guard cells indicated that the effect on s-ORC was due to a lowered intracellular pH, caused by apoplastic acidification. In the hyperpolarized state, the pH-induced depolarization was due to a direct effect of the apoplastic pH on the inward rectifying K⁺ channel. Acidification shifted the threshold potential of the channel to more positive values. This effect was accompanied by a decrease in activation times and an increase of deactivation times, of the channel. From the changes in E_m and membrane conductance, the expected effect of acidification on K⁺ fluxes was calculated. It was concluded that apoplastic acidification will increase the K⁺-efflux in the depolarized state and reduce the K⁺-influx in the hyperpolarized state. Received: 28 April 1997 / Accepted: 10 November 1997     

Impact of the black rhinoceros (Diceros bicornis minor) on a local population of Euphorbia bothae in the Great Fish River Reserve,South Africa

In the Great Fish River Reserve, South Africa, black rhinoceros (Diceros bicornis minor) feed extensively on a local population of Euphorbia bothae. Maintaining the endangered black rhinoceros and the protected E. bothae population are both conservation priorities of the reserve. Therefore, the sustainability of this plant–animal interaction was investigated by comparing population characteristics, browsing incidence and intensity within the reserve and in an adjacent exclosure without access to rhino. Fixed‐point photographs showed that over a 2‐month period 36.6% of 213 monitored plants were browsed, with an average biomass loss of 13%, and 1% were destroyed. Of 26 plants re‐photographed after approximately 3 years, 70% showed a decrease in biomass, averaging 37.8% over this period. In this time span, 19% of the monitored plants died. Small plants (<45 cm) were over‐represented in the rhino‐browsed area, whereas the fraction of reproductively active plants and overall plant density were found to be lower than in the adjacent exclosure. No evidence of short‐term compensatory growth in response to browsing was found for E. bothae. This study indicates that, with the current population size, rhinos are overexploiting the E. bothae population and special measures should be taken to prevent local extinction.     

Association of Lung Inflammatory Cells with Small Airways Function and Exhaled Breath Markers in Smokers – Is There a Specific Role for Mast Cells?

Background

Smoking is associated with a mixed inflammatory infiltrate in the airways. We evaluated whether airway inflammation in smokers is related to lung function parameters and inflammatory markers in exhaled breath.

Methods

Thirty-seven smokers undergoing lung resection for primary lung cancer were assessed pre-operatively by lung function testing including single-breath-nitrogen washout test (sb-N2-test), measurement of fractional exhaled nitric oxide (FeNO) and pH/8-isoprostane in exhaled breath condensate (EBC). Lung tissue sections containing cancer-free large (LA) and small airways (SA) were stained for inflammatory cells. Mucosal (MC_T) respectively connective tissue mast cells (MC_TC) and interleukin-17A (IL-17A) expression by mast cells was analysed using a double-staining protocol.

Results

The median number of neutrophils, macrophages and mast cells infiltrating the lamina propria and adventitia of SA was higher than in LA. Both MCTC and MC_T were higher in the lamina propria of SA compared to LA (MC_TC: 49 vs. 27.4 cells/mm²; MC_T: 162.5 vs. 35.4 cells/mm²; P<0.005 for both instances). IL-17A expression was predominantly detected in MC_TC of LA. Significant correlations were found for the slope of phase III % pred. of the sb-N2-test (r_s= -0.39), for the FEV₁% pred. (r_s= 0.37) and for FEV₁/FVC ratio (r_s=0.38) with MC_T in SA (P<0.05 for all instances). 8-isoprostane concentration correlated with the mast cells in the SA (r_s=0.44), there was no correlation for pH or FeNO with cellular distribution in SA.

Conclusions

Neutrophils, macrophages and mast cells are more prominent in the SA indicating that these cells are involved in the development of small airway dysfunction in smokers. Among these cell types, the best correlation was found for mast cells with lung function parameters and inflammatory markers in exhaled breath. Furthermore, the observed predominant expression of IL-17A in mast cells warrants further investigation to elucidate their role in smoking-induced lung injury, despite the lack of correlation with lung function and exhaled breath parameters.