More pests but less pesticide applications: Ambivalent effect of landscape complexity on conservation biological control

In agricultural landscapes, the amount and organization of crops and semi-natural habitats (SNH) have the potential to promote a bundle of ecosystem services due to their influence on ecological community at multiple spatio-temporal scales. SNH are relatively undisturbed and are often source of complementary resources and refuges, therefore supporting more diverse and abundant natural pest enemies. However, the nexus of SNH proportion and organization with pest suppression is not trivial. It is thus crucial to understand how the behavior of pest and natural enemy species, the underlying landscape structure, and their interaction, may influence conservation biological control (CBC). Here, we develop a generative stochastic landscape model to simulate realistic agricultural landscape compositions and configurations of fields and linear elements. Generated landscapes are used as spatial support over which we simulate a spatially explicit predator-prey dynamic model. We find that increased SNH presence boosts predator populations by sustaining high predator density that regulates and keeps pest density below the pesticide application threshold. However, predator presence over all the landscape helps to stabilize the pest population by keeping it under this threshold, which tends to increase pest density at the landscape scale. In addition, the joint effect of SNH presence and predator dispersal ability among hedge and field interface results in a stronger pest regulation, which also limits pest growth. Considering properties of both fields and linear elements, such as local structure and geometric features, provides deeper insights for pest regulation; for example, hedge presence at crop field boundaries clearly strengthens CBC. Our results highlight that the integration of species behaviors and traits with landscape structure at multiple scales is necessary to provide useful insights for CBC.     

The synthesis of NPQ-effective zeaxanthin depends on the presence of a transmembrane proton gradient and a slightly basic stromal side of the thylakoid membrane

In the present study we address the question which factors during the synthesis of zeaxanthin determine its capacity to act as a non-photochemical quencher of chlorophyll fluorescence. Our results show that zeaxanthin has to be synthesized in the presence of a transmembrane proton gradient. However, it is not essential that the proton gradient is generated by the light-driven electron transport. NPQ-effective zeaxanthin can also be formed by an artificial proton gradient in the dark due to ATP hydrolysis. Zeaxanthin that is synthesized in the dark in the absence of a proton gradient by the low pH-dependent activation of violaxanthin de-epoxidase is not able to induce NPQ. The second important factor during the synthesis of zeaxanthin is the pH-value of the stromal side of the thylakoid membrane. Here we show that the stromal side has to be neutral or slightly basic in order to generate zeaxanthin which is able to induce NPQ. Thylakoid membranes in reaction medium pH 5.2, which experience low pH-values on both sides of the membrane, are unable to generate NPQ-effective zeaxanthin, even in the presence of an additional light-driven proton gradient. Analysing the pigment contents of purified photosystem II light-harvesting complexes we are further able to show that the NPQ ineffectiveness of zeaxanthin formed in the absence of a proton gradient is not caused by changes in its rebinding to the light-harvesting proteins. Purified monomeric and trimeric light-harvesting complexes contain comparable amounts of zeaxanthin when they are isolated from thylakoid membranes enriched in either NPQ-effective or ineffective zeaxanthin.     

Sulfated membrane adsorbers for economic pseudo‐affinity capture of influenza virus particles

Strategies to control outbreaks of influenza, a contagious respiratory tract disease, are focused mainly on prophylactic vaccinations in conjunction with antiviral medications. Currently, several mammalian cell culture‐based influenza vaccine production processes are being established, such as the technologies introduced by Novartis Behring (Optaflu®) or Baxter International Inc. (Celvapan). Downstream processing of influenza virus vaccines from cell culture supernatant can be performed by adsorbing virions onto sulfated column chromatography beads, such as Cellufine® sulfate. This study focused on the development of a sulfated cellulose membrane (SCM) chromatography unit operation to capture cell culture‐derived influenza viruses. The advantages of the novel method were demonstrated for the Madin Darby canine kidney (MDCK) cell‐derived influenza virus A/Puerto Rico/8/34 (H1N1). Furthermore, the SCM‐adsorbers were compared directly to column‐based Cellufine® sulfate and commercially available cation‐exchange membrane adsorbers. Sulfated cellulose membrane adsorbers showed high viral product recoveries. In addition, the SCM‐capture step resulted in a higher reduction of dsDNA compared to the tested cation‐exchange membrane adsorbers. The productivity of the SCM‐based unit operation could be significantly improved by a 30‐fold increase in volumetric flow rate during adsorption compared to the bead‐based capture method. The higher flow rate even further reduced the level of contaminating dsDNA by about twofold. The reproducibility and general applicability of the developed unit operation were demonstrated for two further MDCK cell‐derived influenza virus strains: A/Wisconsin/67/2005 (H3N2) and B/Malaysia/2506/2004. Overall, SCM‐adsorbers represent a powerful and economically favorable alternative for influenza virus capture over conventional methods using Cellufine® sulfate. Biotechnol. Bioeng. 2009;103: 1144–1154. © 2009 Wiley Periodicals, Inc.     

A New Paradigm for MAPK: Structural Interactions of hERK1 with Mitochondria in HeLa Cells

Extracellular signal-regulated protein kinase 1 and 2 (ERK1/2) are members of the MAPK family and participate in the transduction of stimuli in cellular responses. Their long-term actions are accomplished by promoting the expression of specific genes whereas faster responses are achieved by direct phosphorylation of downstream effectors located throughout the cell. In this study we determined that hERK1 translocates to the mitochondria of HeLa cells upon a proliferative stimulus. In the mitochondrial environment, hERK1 physically associates with (i) at least 5 mitochondrial proteins with functions related to transport (i.e. VDAC1), signalling, and metabolism; (ii) histones H2A and H4; and (iii) other cytosolic proteins. This work indicates for the first time the presence of diverse ERK-complexes in mitochondria and thus provides a new perspective for assessing the functions of ERK1 in the regulation of cellular signalling and trafficking in HeLa cells.     

The NLRP3 inflammasome is differentially activated by pneumolysin variants and contributes to host defense in pneumococcal pneumonia

Streptococcus pneumoniae is a leading cause of pneumonia, meningitis, and sepsis. Pneumococci can be divided into >90 serotypes that show differences in the pathogenicity and invasiveness. We tested the hypotheses that the innate immune inflammasome pathway is involved in fighting pneumococcal pneumonia and that some invasive pneumococcal types are not recognized by this pathway. We show that human and murine mononuclear cells responded to S. pneumoniae expressing hemolytic pneumolysin by producing IL-1β. This IL-1β production depended on the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome. Some serotype 1, serotype 8, and serotype 7F bacteria, which have previously been associated with increased invasiveness and with production of toxins with reduced hemolytic activity, or bacterial mutants lacking pneumolysin did not stimulate notable IL-1β production. We further found that NLRP3 was beneficial for mice during pneumonia caused by pneumococci expressing hemolytic pneumolysin and was involved in cytokine production and maintenance of the pulmonary microvascular barrier. Overall, the inflammasome pathway is protective in pneumonia caused by pneumococci expressing hemolytic toxin but is not activated by clinically important pneumococcal sequence types causing invasive disease. The study indicates that a virulence factor polymorphism may substantially affect the recognition of bacteria by the innate immune system.     

Model studies for the direct effect of high-energy irradiation on DNA. Mechanism of strand break formation induced by laser photoionization of poly U in aqueous solution

Laser flash photolysis of polyuridylic acid (poly U) in anoxic aqueous solutions leads to biphotonic photoionization of the uracil moiety followed by the formation of single strand breaks (ssb). The rate constant for ssb formation (1.0 s-1, obtained from the slow component of conductivity increase at 23 degrees C and pH 6.8) increases with decreasing pH to 235 s-1 at pH 3.5. The activation energy (pre-exponential factor) was measured to be 66 kJ mol-1 (5 X 10(11) s-1) at pH 6.8. Addition of dithiothreitol (DTT) or glutathione (GSH) prevents ssb formation by reacting with a poly U intermediate (rate constant = 1.2 X 10(6) and 0.16 X 10(6) dm3 mol-1 s-1, respectively). Since with OH radicals as initiators very similar data have been obtained for the kinetics of ssb formation and for the reaction with DTT, we conclude that photoionization of the uracil moiety in poly U leads eventually to the same chemical pathway for ssb formation as that induced by OH radicals. Furthermore, we propose that protection by DTT and GSH occurs via H donation to the C-4' radicals of the sugar moiety of DNA and to the C-4' and the C-2' radicals of poly U.