Host plant specialization driven by sexual selection

We propose a new mechanism based on sexual selection to explain the evolution of diet breadth in insects. More specifically, we show that mate choice in females for certain diet-derived male pheromones can be exploited by maternal effect genes that preferentially place offspring on a specific host plant, resulting in specialization. Our analytical model also suggests that the process is more likely to occur with species that show male-congregating mating strategies, such as lekking and hilltopping. The model offers a new explanation for the similarity between the composition of male lepidopteran pheromones and the chemistry of their host plants and also suggests a novel mechanism of host plant shift. This is the first time that sexual selection has been proposed to drive host plant specialization and the first time that a mechanism with selection acting solely on the adult stage has been shown to be capable of determining larval feeding habits.     

First outbreak reported caused by Erysipelothrix species strain 2 in turkeys from poultry-producing farms in Brazil

Purpose

The aims of this study were to report the first isolation of Erysipelothrix sp. strain 2 (ES2) associated with clinical signs of diseases as well as mortality in turkeys and identify the antimicrobial resistance of the isolates.

Methods

We evaluated 118 farms for bacteriological analysis and TaqMan real-time PCR to identify the microorganism in different organs. After this, we made the epidemiological analysis between the positive flocks and the mortality mean. We performed the sequencing of the 16S rRNA region and the assessment of antimicrobial resistance.

Results

We have identified 18 (15.25%) as ES2-positive flocks, without any other species from the same genus being found. After analysing the organ samples, we found liver as the organ of choice for the isolation of the ES2. The sequencing of 16S rRNA region of ES2 identified high homology with E. tonsillarum and E. rhusiopathiae, suggesting that it is not the best-suited target to identify this species. We have found a positive association between isolation of the bacteria in organs and flocks’ mortality. Positive flocks had a mortality mean rate of 6.87%, which is significantly greater than 3.76% in negative flocks. Ill turkeys had gross lesions of generalized septicaemia. The bacterial isolates showed high resistance to fosfomycin and trimethoprim/sulfamethoxazole and sensibility to norfloxacin, amoxicillin and lincomycin/spectinomycin.

Conclusion

This is the first study in the world that addressed ES2 as the causative agent of erysipelas in turkey.

     

Synphilin-1 enhances α-synuclein aggregation in yeast and contributes to cellular stress and cell death in a Sir2-dependent manner

Background

Parkinson''s disease is characterized by the presence of cytoplasmic inclusions, known as Lewy bodies, containing both aggregated α-synuclein and its interaction partner, synphilin-1. While synphilin-1 is known to accelerate inclusion formation by α-synuclein in mammalian cells, its effect on cytotoxicity remains elusive.

Methodology/Principal Findings

We expressed wild-type synphilin-1 or its R621C mutant either alone or in combination with α-synuclein in the yeast Saccharomyces cerevisiae and monitored the intracellular localization and inclusion formation of the proteins as well as the repercussions on growth, oxidative stress and cell death. We found that wild-type and mutant synphilin-1 formed inclusions and accelerated inclusion formation by α-synuclein in yeast cells, the latter being correlated to enhanced phosphorylation of serine-129. Synphilin-1 inclusions co-localized with lipid droplets and endomembranes. Consistently, we found that wild-type and mutant synphilin-1 interacts with detergent-resistant membrane domains, known as lipid rafts. The expression of synphilin-1 did not incite a marked growth defect in exponential cultures, which is likely due to the formation of aggresomes and the retrograde transport of inclusions from the daughter cells back to the mother cells. However, when the cultures approached stationary phase and during subsequent ageing of the yeast cells, both wild-type and mutant synphilin-1 reduced survival and triggered apoptotic and necrotic cell death, albeit to a different extent. Most interestingly, synphilin-1 did not trigger cytotoxicity in ageing cells lacking the sirtuin Sir2. This indicates that the expression of synphilin-1 in wild-type cells causes the deregulation of Sir2-dependent processes, such as the maintenance of the autophagic flux in response to nutrient starvation.

Conclusions/Significance

Our findings demonstrate that wild-type and mutant synphilin-1 are lipid raft interacting proteins that form inclusions and accelerate inclusion formation of α-synuclein when expressed in yeast. Synphilin-1 thereby induces cytotoxicity, an effect most pronounced for the wild-type protein and mediated via Sir2-dependent processes.     

Limits and Trade-Offs of Topological Network Robustness

We investigate the trade-off between the robustness against random and targeted removal of nodes from a network. To this end we utilize the stochastic block model to study ensembles of infinitely large networks with arbitrary large-scale structures. We present results from numerical two-objective optimization simulations for networks with various fixed mean degree and number of blocks. The results provide strong evidence that three different blocks are sufficient to realize the best trade-off between the two measures of robustness, i.e. to obtain the complete front of Pareto-optimal networks. For all values of the mean degree, a characteristic three block structure emerges over large parts of the Pareto-optimal front. This structure can be often characterized as a core-periphery structure, composed of a group of core nodes with high degree connected among themselves and to a periphery of low-degree nodes, in addition to a third group of nodes which is disconnected from the periphery, and weakly connected to the core. Only at both extremes of the Pareto-optimal front, corresponding to maximal robustness against random and targeted node removal, a two-block core-periphery structure or a one-block fully random network are found, respectively.     

The ruthenium complexes cis-(dichloro)tetramineruthenium(III) chloride and cis-tetraammine(oxalato)ruthenium(III) dithionate overcome resistance inducing apoptosis on human lung carcinoma cells (A549)

Lung cancer is one of the leading causes of death in the world, and non-small cell lung carcinoma accounts for approximately 75–85 % of all lung cancers. In the present work, we studied the antitumor activity of the compound cis-(dichloro)tetramineruthenium(III) chloride {cis-[RuCl₂(NH₃)₄]Cl} against human lung carcinoma tumor cell line A549. The present study aimed to investigate the relationship between the expression of MDR1 and CYP450 genes in human lung carcinoma cell lines A549 treated with cisCarboPt, cisCRu(III) and cisDRu(III). The ruthenium-based coordinated complexes presented low cytotoxic and antiproliferative activities, with high IC₅₀ values, 196 (±15.49), 472 (±20.29) and 175 (±1.41) for cisCarboPt, cisCRu(III) and cisDRu(III), respectively. The tested compounds induced apoptosis in A549 tumor cells as evidenced by caspase 3 activation, but only at high concentrations. Results also revealed that the amplification of P-gp gene is greater in A549 cells exposed to cisCarboPt and cisCRu(III) than cisDRu(III). Taken together all these results strongly demonstrate that MDR-1 over-expression in A549 cells could be associated to a MDR phenotype of these cells and moreover, it is also contributing to the platinum, and structurally-related compound, resistance in these cells. The identification and characterization of novel mechanisms of drug resistance will enable the development of a new generation of anti-cancer drugs that increase cancer sensitivity and/or represent more effective chemotherapeutic agents.     

Human carboxylesterase 2: Studies on the role of glycosylation for enzymatic activity

Human carboxylesterase 2 (hCES2) is a glycoprotein involved in the metabolism of drugs and several environmental xenobiotics, whose crystallization has been proved to be a challenging task. This limitation could partly be due to glycosylation heterogeneity and has delayed the disclosure of the 3D structure of hCES2 which would be of upmost relevance for the development of new substrates and inhibitors. The present work evaluated the involvement of glycans in hCES2 activity and thermo stability in an attempt to find alternative active forms of the enzyme that might be adequate for structure elucidation.Partial or non-glycosylated forms of a secreted form of hCES2 have been obtained by three approaches: (i) enzymatic deglycosylation with peptide N-glycosidase F; (ii) incubation with the inhibitor tunicamycin; ii) site directed mutagenesis of each or both N-glycosylation sites.Deglycosylated protein did not show a detectable decrease in enzyme activity. On the other hand, tunicamycin led to decreased levels of secreted hCES2 but the enzyme was still active. In agreement, mutation of each and both N-glycosylation sites led to decreased levels of secreted active hCES2. However, the thermostability of the glycosylation mutants was decreased.The results indicated that glycans are involved, to some extent in protein folding in vivo, however, removal of glycans does not abrogate the activity of secreted hCES2.     

Pseudotumoral presentation of chronic pulmonary paracoccidioidomycosis: Report of a case

A case of unilateral paracoccidioidal pulmonary lesion simulating a neoplasm is reported.This case was presented on the XVII World Congress on Diseases of the Chest, Amsterdam, The Netherland, June 1993.