Finding its place in a competitive ant community: leaf fidelity of <Emphasis Type="Italic">Camponotus sericeus</Emphasis>

Summary. Many species of ground nesting ants regularly visit extrafloral nectaries (EFNs) of the savannah tree Pseudocedrela kotschyi. The distribution of ants on the plants is mosaic-like, i.e. stable and predictable with different ant species dominating neighbouring trees. In order to examine whether foraging behaviour may influence the structure of these ant communities, we investigated individual foraging behaviour of Camponotus sericeus, the ant species with highest incidence on P. kotschyi trees in the study area. Foragers of C. sericeus continuously visited EFNs on the leafs of P. kotschyi during their diurnal activity period. Individually marked foragers showed a pronounced fidelity for individual plants and particular leaves. Ant individuals returned to the same plants over a three week period at least. They persistently focused foraging on the same leaves (about three per ant). Null model analysis of ant distribution revealed that ants partitioned their host plant. Co-occurrence on the same leaves was significantly lower than could be expected by chance for most trees studied. Foraging was not oriented towards the plants growing closest to the nest but more distantly growing plants were considerably used. Choice of plants could therefore be influenced by plant quality or by presence of other, competing ant species. The study is the first to show leaf fidelity caused by EFNs and micro-site fidelity within the context of species rich ant communities. It considers the resulting systematic, partitioned use of individual plants as important factor supporting the formation of a mosaic-like ant distribution on plants.     

Biosorption of Cr(VI) onto marine Aspergillus niger: experimental studies and pseudo-second order kinetics

The removal of hexavalent chromium from aqueous solution was studied in batch experiments using dead biomass of three different species of marine Aspergillus after alkali treatment. All the cultures exhibited potential to remove Cr(VI), out of which, Aspergillus niger was found to be the most promising one. This culture was further studied employing variation in pH, temperature, metal ion concentration and biomass concentration with a view to understand the effect of these parameters on biosorption of Cr(VI). Higher biosorption percentage was evidenced at lower initial concentration of Cr(VI) ion, while the sorption capacity of the biomass increased with rising concentration of ions. Biomass as low as 0.8 g l⁻¹ could biosorb 95% Cr(VI) ions within 2,880 min from an aqueous solution of 400 mg l⁻¹ Cr(VI) concentration. Optimum pH and temperature for Cr(VI) biosorption were 2.0 and 50°C, respectively. Kinetic studies based on pseudo second order models like Sobkowsk and Czerwinski, Ritchie, Blanchard and Ho and Mckay rate expressions have also been carried out. The nature of the possible cell–metal ion interactions was evaluated by FTIR, SEM and EDAX analysis.     

Deletion of ghrelin prevents aging‐associated obesity and muscle dysfunction without affecting longevity

During aging, decreases in energy expenditure and locomotor activity lead to body weight and fat gain. Aging is also associated with decreases in muscle strength and endurance leading to functional decline. Here, we show that lifelong deletion of ghrelin prevents development of obesity associated with aging by modulating food intake and energy expenditure. Ghrelin deletion also attenuated the decrease in phosphorylated adenosine monophosphate‐activated protein kinase (pAMPK) and downstream mediators in muscle, and increased the number of type IIa (fatigue resistant, oxidative) muscle fibers, preventing the decline in muscle strength and endurance seen with aging. Longevity was not affected by ghrelin deletion. Treatment of old mice with pharmacologic doses of ghrelin increased food intake, body weight, and muscle strength in both ghrelin wild‐type and knockout mice. These findings highlight the relevance of ghrelin during aging and identify a novel AMPK‐dependent mechanism for ghrelin action in muscle.     

QTL analysis for aphid resistance and growth traits in apple

The rosy apple aphid (Dysaphis plantaginea), the leaf-curling aphid (Dysaphis cf. devecta) and the green apple aphid (Aphis pomi) are widespread pest insects that reduce growth of leaves, fruits and shoots in apple (Malus × domestica). Aphid control in apple orchards is generally achieved by insecticides, but alternative management options like growing resistant cultivars are needed for a more sustainable integrated pest management (IPM). A linkage map available for a segregating F₁-cross of the apple cultivars ‘Fiesta’ and ‘Discovery’ was used to investigate the genetic basis of resistance to aphids. Aphid infestation and plant growth characteristics were repeatedly assessed for the same 160 apple genotypes in three different environments and 2 consecutive years. We identified amplified fragment length polymorphism (AFLP) markers linked to quantitative trait loci (QTLs) for resistance to D. plantaginea (‘Fiesta’ linkage group 17, locus 57.7, marker E33M35–0269; heritability: 28.3%), and to D. cf. devecta (‘Fiesta’ linkage group 7, locus 4.5, marker E32M39–0195; heritability: 50.2%). Interactions between aphid species, differences in climatic conditions and the spatial distribution of aphid infestation were identified as possible factors impeding the detection of QTLs. A pedigree analysis of simple sequence repeat (SSR) marker alleles closely associated with the QTL markers revealed the presence of the alleles in other apple cultivars with reported aphid resistance (‘Wagener’, ‘Cox’s Orange Pippin’), highlighting the genetic basis and also the potential for gene pyramiding of aphid resistance in apple. Finally, significant QTLs for shoot length and stem diameter were identified, while there was no relationship between aphid resistance and plant trait QTLs. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users.     

Extrasynaptic GABAA receptors in the crosshairs of hormones and ethanol

Gamma-aminobutyric acid (GABA) is the main chemical inhibitory neurotransmitter in the brain. In the central nervous system (CNS) it acts on two distinct types of receptor: an ion channel, i.e., an "ionotropic" receptor permeable to Cl- and HCO3- (GABAA receptors) and a G-protein coupled "metabotropic" receptor that is linked to various effector mechanisms (GABAB receptors). This review will summarize novel developments in the physiology and pharmacology of GABAA receptors (GABAARs), specifically those found outside synapses. The focus will be on a particular combination of GABAAR subunits sensitive to ovarian and adrenal cortical steroid hormone metabolites that are synthesized in the brain (neurosteroids) and to sobriety impairing concentrations of ethanol. These receptors may be the final common pathway for interactions between ethanol and ovarian and stress-related neurosteroids.     

Decreased clearance of serum retinol-binding protein and elevated levels of transthyretin in insulin-resistant ob/ob mice

Serum retinol-binding protein (RBP4) is secreted by liver and adipocytes and is implicated in systemic insulin resistance in rodents and humans. RBP4 normally binds to the larger transthyretin (TTR) homotetramer, forming a protein complex that reduces renal clearance of RBP4. To determine whether alterations in RBP4-TTR binding contribute to elevated plasma RBP4 levels in insulin-resistant states, we investigated RBP4-TTR interactions in leptin-deficient ob/ob mice and high-fat-fed obese mice (HFD). Gel filtration chromatography of plasma showed that 88-94% of RBP4 is contained within the RBP4-TTR complex in ob/ob and lean mice. Coimmunoprecipitation with an RBP4 antibody brought down stoichiometrically equal amounts of TTR and RBP4, indicating that TTR was not more saturated with RBP4 in ob/ob mice than in controls. However, plasma TTR levels were elevated approximately fourfold in ob/ob mice vs. controls. RBP4 injected intravenously in lean mice cleared rapidly, whereas the t(1/2) for disappearance was approximately twofold longer in ob/ob plasma. Urinary fractional excretion of RBP4 was reduced in ob/ob mice, consistent with increased retention. In HFD mice, plasma TTR levels and clearance of injected RBP4 were similar to chow-fed controls. Hepatic TTR mRNA levels were elevated approximately twofold in ob/ob but not in HFD mice. Since elevated circulating RBP4 causes insulin resistance and glucose intolerance in mice, these findings suggest that increased TTR or alterations in RBP4-TTR binding may contribute to insulin resistance by stabilizing RBP4 at higher steady-state concentrations in circulation. Lowering TTR levels or interfering with RBP4-TTR binding may enhance insulin sensitivity in obesity and type 2 diabetes.     

Molecular determinants for the differential coupling of Galpha(16) to the melatonin MT1, MT2 and Xenopus Mel1c receptors

The pineal neurohormone melatonin modulates a variety of physiological processes through different receptors. It has recently been reported that the cloned melatonin receptors (MT1, MT2 and Mel1c) exhibit differential abilities to stimulate phospholipase C (PLC) via G(16). Here we examined the molecular basis of such differences in melatonin receptor signaling. Coexpression of MT1 or MT2 with the alpha subunit of G(16) (Galpha(16) ) allowed COS-7 cells to accumulate inositol phosphates in response to 2-iodomelatonin. In contrast, Mel1c did not activate Galpha(16) even though its expression was demonstrated by radioligand binding and agonist-induced inhibition of adenylyl cyclase. As Mel1c possesses an exceptionally large C-terminal tail, we further asked if this structural feature prevented productive coupling to Galpha(16). Eleven chimeric melatonin or mutant receptors were constructed by swapping all or part of the C-terminal tail between MT1, MT2 and Mel1c. All chimeras were fully capable of binding 2-[(125) I]iodomelatonin and inhibiting adenylyl cyclase. Chimeras containing the full-length Mel1c tail were incapable of activating Galpha(16), while those that contained the complete C-terminal region of either MT1 or MT2 stimulated PLC. Incorporation of the extra portion of the C-terminal tail of Mel1c to either MT1 or MT2 completely abolished the chimeras' ability to stimulate PLC via Galpha(16). In contrast, truncation of the C-terminal tail of Mel1c allowed interaction with Galpha(16). Our results suggest that Galpha(16) can discern structural differences amid the three melatonin receptors and provide evidence for functional distinction of Mel1c from MT1 and MT2 receptors.     

Comparison of single NMDA receptor channels recorded on hippocampal principal cells and oriens/alveus interneurons projecting to stratum lacunosum-moleculare (O-LM cells)

NMDA receptors participate in the glutamatergic excitation of both principal cells and GABAergic interneurons. The features of NMDA channels on specific interneurons, however, are not known. Therefore, we obtained direct measurements of single NMDA receptor channels on anatomically identified oriens/alveus interneurons projecting to stratum lacunosum-moleculare (O-LM cells) and compared them to those found on hippocampal principal cells using cell-attached recordings in in vitro slice preparations. The recorded channels could be blocked by ketamine, a membrane-permeable NMDA channel inhibitor. In the absence of Mg(2+), all O-LM cells had NMDA channels with a comparable slope conductance (approximately 60pS) to those measured on CA1 pyramidal cells or dentate granule cells. In addition, NMDA channels with smaller conductance (43-45 pS) were also found on two O-LM cells but not on principal cells. These results suggest that at least two types of NMDA channels are expressed on O-LM cells likely reflecting distinct subunit composition.     

Quantification of platelet activation status by analyzing P-selectin expression

Platelet activation status (PAS) is used for characterizing quality and function of platelets in various experimental and clinical settings. In this study, we created a set of platelet populations differing in PAS, using stimulation of platelets with thrombin in a wide range of concentrations, and analyzed a number of flow cytometric parameters, which characterize PAS by measuring P-selectin (CD62) expression. We found that PAS of a platelet population depends significantly on the specific parameters used for detecting CD62 expression and can differ several fold. We revealed the parameters which are more sensitive for distinguishing the differences between populations with similar low and similar high PAS. Selection of valid and sensitive flow cytometric parameters for PAS evaluation and distinguishing the differences between platelet populations with similar PAS can serve for diagnosis of platelet-associated disorders and monitoring their course and therapeutic interventions.     

Perforin-dependent cryptococcal microbicidal activity in NK cells requires PI3K-dependent ERK1/2 signaling

Previously, NK cells have been reported to kill the opportunistic fungal pathogen Cryptococcus neoformans through a perforin-dependent mechanism; however, the receptor and signaling involved are unknown. In this report we sought to identify the signaling pathways activated and required for direct perforin-mediated killing of microbes. In this study, using the NK-like cell line YT and primary peripheral blood NK cells, it is demonstrated that YT cells kill C. neoformans and that the killing is accompanied by the activation of PI3K. We demonstrate that inhibition of either the catalytic subunit (using a pharmacological inhibitor) or the alpha-regulatory subunit (using small interfering RNA knockdown) of PI3K significantly inhibited the killing of C. neoformans. Downstream of PI3K, ERK1/2 was activated in a PI3K-dependent fashion and was required for cryptococcal killing. Furthermore, we demonstrate that perforin release from YT cells can be detected by 4 h after contact of the YT cells with C. neoformans and that the release of perforin is blocked by pharmacological inhibition of either PI3K or ERK1/2. Defective degranulation is rooted in the inability to polarize perforin-containing granules toward the target. Finally, we demonstrate that PI3K-ERK1/2-dependent signaling is activated and required for the killing of C. neoformans by primary NK cells. Taken together, these data identify a conserved PI3K-ERK1/2 pathway that is used by NK cells during the direct killing of C. neoformans and demonstrate that the pathway is essential in the formation and activation of the microbicidal mechanism.