Cloning and overexpression of antifungal barley chitinase gene in Escherichia coli

Plant chitinases are pathogenesis-related proteins, which are believed to be involved in plant defense responses to pathogen infection. In this study, chitinase gene from barley was cloned and overexpressed in Escherichia coli. Chitinase (35 kDa) was isolated and purified. Since the protein was produced as insoluble inclusion bodies, the protein was solubilized and refolded. Purified chitinase exerted broad-spectrum antifungal activity against Botrytis cinerea (blight of tobacco), Pestalotia theae (leaf spot of tea), Bipolaris oryzae (brown spot of rice), Alternaria sp. (grain discoloration of rice), Curvularia lunata (leaf spot of clover) and Rhizoctonia solani (sheath blight of rice). Due to the potential of broad-spectrum antifungal activity barley chitinase gene can be used to enhance fungal-resistance in crop plants such as rice, tobacco, tea and clover.     

The vicious cycle of apoptotic beta-cell death in type 1 diabetes

Autoimmune insulitis, the cause of type 1 diabetes, evolves through several discrete stages that culminate in beta-cell death. In the first stage, antigenic epitopes of B-cell-specific peptides are processed by antigen presenting cells in local lymph nodes, and auto-reactive lymphocyte clones are propagated. Subsequently, cell-mediated and direct cytokine-mediated reactions are generated against the beta-cells, and the beta-cells are sensitized to apoptosis. Ironically, the beta-cells themselves contribute some of the cytokines and chemokines that provoke the immune reaction within the islets. Once this vicious cycle of autoimmunity is fully developed, the fate of the beta-cells in the islets is sealed, and clinical diabetes inevitably ensues. Differences in various aspects of these concurrent events appear to underlie the significant discrepancies in experimental data observed in experimental models that simulate autoimmune insulitis.     

LTP inhibits LTD in the hippocampus via regulation of GSK3beta

Glycogen synthase kinase-3 (GSK3) has been implicated in major neurological disorders, but its role in normal neuronal function is largely unknown. Here we show that GSK3beta mediates an interaction between two major forms of synaptic plasticity in the brain, N-methyl-D-aspartate (NMDA) receptor-dependent long-term potentiation (LTP) and NMDA receptor-dependent long-term depression (LTD). In rat hippocampal slices, GSK3beta inhibitors block the induction of LTD. Furthermore, the activity of GSK3beta is enhanced during LTD via activation of PP1. Conversely, following the induction of LTP, there is inhibition of GSK3beta activity. This regulation of GSK3beta during LTP involves activation of NMDA receptors and the PI3K-Akt pathway and disrupts the ability of synapses to undergo LTD for up to 1 hr. We conclude that the regulation of GSK3beta activity provides a powerful mechanism to preserve information encoded during LTP from erasure by subsequent LTD, perhaps thereby permitting the initial consolidation of learnt information.     

Conservative N cycling despite high atmospheric deposition in early successional African tropical lowland forests

Plant and Soil - Many applied disciplines have recognized problems related to the practice of data analysis within their own communities. Some of them have even declared the existence of a...     

The ratio of acetate‐to‐glucose oxidation in astrocytes from a single 13C NMR spectrum of cerebral cortex

The ¹³C‐labeling patterns in glutamate and glutamine from brain tissue are quite different after infusion of a mixture of ¹³C‐enriched glucose and acetate. Two processes contribute to this observation, oxidation of acetate by astrocytes but not neurons, and preferential incorporation of α‐ketoglutarate into glutamate in neurons, and incorporation of α‐ketoglutarate into glutamine in astrocytes. The acetate:glucose ratio, introduced previously for analysis of a single ¹³C NMR spectrum, provides a useful index of acetate and glucose oxidation in the brain tissue. However, quantitation of relative substrate oxidation at the cell compartment level has not been reported. A simple mathematical method is presented to quantify the ratio of acetate‐to‐glucose oxidation in astrocytes, based on the standard assumption that neurons do not oxidize acetate. Mice were infused with [1,2‐¹³C]acetate and [1,6‐¹³C]glucose, and proton decoupled ¹³C NMR spectra of cortex extracts were acquired. A fit of those spectra to the model indicated that ¹³C‐labeled acetate and glucose contributed approximately equally to acetyl‐CoA (0.96) in astrocytes. As this method relies on a single ¹³C NMR spectrum, it can be readily applied to multiple physiologic and pathologic conditions.

     

Is allometry of sexual traits adaptive? A field test with territorial damselflies

Recent studies have linked static allometry of sexual traits to selective advantages, in terms of sexual selection. An underlying, yet untested, assumption is that the allometry of sexual traits confers higher mating success and/or survival. Here, we investigated whether the allometry of two sexual traits is related to male mating success and survival in two species of damselflies: wing size in Paraphlebia zoe and the red‐pigmented wing spot in Hetaerina americana. We used large field‐based data sets of marked‐recaptured animals, in which we recorded male mating success and survival. Both sexual traits exhibited hyperallometric patterns; however, allometry was not linked to either mating success or survival. These results indicate that, at least during the period of sexual competition, allometry does not seem to be adaptive. Although our results may only apply to our damselfly study subjects (which nevertheless would require further tests in different seasons and/or study sites), our findings should encourage researchers to evaluate at least whether the assumed adaptiveness of sexual trait allometry holds for their study animals. © 2015 The Linnean Society of London, Biological Journal of the Linnean Society, 2015, 114 , 327–334.     

The struggle for safety: effectiveness of caterpillar defenses against bird predation

The effectiveness of anti‐predator traits, such as warning signals and camouflage, has rarely been quantified from a phylogenetic community ecology perspective. Here we use a phylogenetic comparative analysis to test the association between several putative anti‐predator traits and bird predation risk in an assemblage of caterpillar species. We synthesize eight years of field and laboratory study of a temperate forest community, including a four‐year bird exclusion experiment that provided comparative measures of bird predation risk for 38 caterpillar species from a phylogenetic community. We then conducted a phylogenetic generalized least‐squares and information‐theoretic model selection analysis of warning signals (aposematism or mimicry), camouflage (crypsis or masquerade), and behavioral responses to physical attack as predictors of bird predation, while also accounting for putatively important effects of the abundance, mean body size, and phenology of caterpillar species. The most behaviorally specialized caterpillar species possessing warning signals experienced the lowest bird predation risk, supporting aposematism theory and highlighting the role of prey behavior in the visual signaling of predators. Among the camouflaged caterpillar species, those with the greatest latency to detection by human proxy predators experienced the lowest bird predation risk, supporting camouflage theory. Caterpillar behavioral responses to physical attack, however, predicted increased bird predation risk among camouflaged caterpillars. Although caterpillar abundance, body size, and phenology were expected to be important based on inference from optimal foraging theory and previous field observations, these factors had limited predictive power. This study provides methodologically unique evidence for the importance of morphological and behavioral components of primary, visual defenses of caterpillars against their avian predators in a natural community.