Cleptoparasites, social parasites and a common host: Chemical insignificance for visiting host nests, chemical mimicry for living in

Social insect colonies contain attractive resources for many organisms. Cleptoparasites sneak into their nests and steal food resources. Social parasites sneak into their social organisations and exploit them for reproduction. Both cleptoparasites and social parasites overcome the ability of social insects to detect intruders, which is mainly based on chemoreception. Here we compared the chemical strategies of social parasites and cleptoparasites that target the same host and analyse the implication of the results for the understanding of nestmate recognition mechanisms. The social parasitic wasp Polistes atrimandibularis (Hymenoptera: Vespidae), and the cleptoparasitic velvet ant Mutilla europaea (Hymenoptera: Mutillidae), both target the colonies of the paper wasp Polistes biglumis (Hymenoptera: Vespidae). There is no chemical mimicry with hosts in the cuticular chemical profiles of velvet ants and pre-invasion social parasites, but both have lower concentrations of recognition cues (chemical insignificance) and lower proportions of branched alkanes than their hosts. Additionally, they both have larger proportions of alkenes than their hosts. In contrast, post-invasion obligate social parasites have proportions of branched hydrocarbons as large as those of their hosts and their overall cuticular profiles resemble those of their hosts. These results suggest that the chemical strategies for evading host detection vary according to the lifestyles of the parasites. Cleptoparasites and pre-invasion social parasites that sneak into host colonies limit host overaggression by having few recognition cues, whereas post-invasion social parasites that sneak into their host social structure facilitate social integration by chemical mimicry with colony members.     

Absence of inspiratory laryngeal constrictor muscle activity during nasal neurally adjusted ventilatory assist in newborn lambs

In nonsedated newborn lambs, nasal pressure support ventilation (nPSV) can lead to an active glottal closure in early inspiration, which can limit lung ventilation and divert air into the digestive system, with potentially deleterious consequences. During volume control ventilation (nVC), glottal closure is delayed to the end of inspiration, suggesting that it is reflexly linked to the maximum value of inspiratory pressure. Accordingly, the aim of the present study was to test whether inspiratory glottal closure develops at the end of inspiration during nasal neurally adjusted ventilatory assist (nNAVA), an increasingly used ventilatory mode where maximal pressure is also reached at the end of inspiration. Polysomnographic recordings were performed in eight nonsedated, chronically instrumented lambs, which were ventilated with progressively increasing levels of nPSV and nNAVA in random order. States of alertness, diaphragm, and glottal muscle electrical activity, tracheal pressure, Spo(2), tracheal Pet(CO(2)), and respiratory inductive plethysmography were continuously recorded. Although phasic inspiratory glottal constrictor electrical activity appeared during nPSV in 5 of 8 lambs, it was never observed at any nNAVA level in any lamb, even at maximal achievable nNAVA levels. In addition, a decrease in Pco(2) was neither necessary nor sufficient for the development of inspiratory glottal constrictor activity. In conclusion, nNAVA does not induce active inspiratory glottal closure, in contrast to nPSV and nVC. We hypothesize that this absence of inspiratory activity is related to the more physiological airway pressurization during nNAVA, which tightly follows diaphragm electrical activity throughout inspiration.     

Measures to reduce population fragmentation by roads: what has worked and how do we know?

Roads impede animal movement, which decreases habitat accessibility and reduces gene flow. Ecopassages have been built to mitigate this but there is little research with which to evaluate their effectiveness, owing to the difficulty in accessing results of existing research; the lack of scientific rigor in these studies; and the low priority of connectivity planning in road projects. In this article, we suggest that the imperative for improving studies of ecopassage effectiveness is that road ecology research should be included from the earliest stages of road projects onwards. This would enable before-after-control-impact (BACI) design research, producing useful information for the particular road project as well as rigorous results for use in future road mitigation. Well-designed studies on ecopassage effectiveness could help improve landscape connectivity even with the increasing number and use by traffic of roads.     

Effect of the A30P mutation on the structural dynamics of micelle-bound αSynuclein released in water: a molecular dynamics study

Atomistic molecular dynamics simulation has been used to probe the effect of the A30P mutation on the structural dynamics of micelle-bound, helical αSynuclein when released in an aqueous environment. On the timescales simulated, the effect of the mutation on the secondary structure is restricted to local changes close to the mutation site in the N-terminal helical domain. The changes are transient, and all residues except Lys23 recover their initial structure. The local behavior due to the mutation gives rise to a global difference in the A30P mutant in the form of a permanent kink in the N-terminal helical domain.     

Transfer RNA-dependent asparagine biosynthesis in Gluconacetobacter diazotrophicus and its influence on biological nitrogen fixation

Background and aims

Gluconacetobacter diazotrophicus is a nitrogen-fixing endophytic bacterium isolated from sugarcane, rice, elephant grass, sweet potato, coffee, and pineapple. These plants have high level of asparagine, which promotes microbial growth and inhibits nitrogenase activity. The regulation of intracellular concentrations of this amino acid is essential for growth and biological nitrogen fixation (BNF) in this diazotroph; however its asparagine metabolic pathway has not yet been clearly established.

Methods

The work reported here is the first to demonstrate the use of an alternative route for asparaginyl-tRNA (Asn-tRNA) and asparagine formation in an endophytic nitrogen-fixing bacterium by using in silico and in vitro analysis.

Results

The indirect route involves transamidation of incorrectly charged tRNA via GatCAB transamidase. Nitrogenase activity was completely inhibited by 20?mM Asn in LGI-P medium, which in contrast promotes protein synthesis and microbial growth.

Conclusions

The analysis carried out in this work shows that intracellular levels of asparagine regulate the expression of nitrogenase nifD gene (GDI0437), suggesting that the presence of an alternative route to produce asparagine might give the G. diazotrophicus a tighter control over cell growth and BNF, and may be of importance in the regulation of the endophytic plant-microbe interaction.     

Biogeography revisited with network theory: retracing the history of hydrothermal vent communities

Defining biogeographic provinces to understand the history and evolution of communities associated with a given kind of ecosystem is challenging and usually requires a priori assumptions to be made. We applied network theory, a holistic and exploratory method, to the most complete database of faunal distribution available on oceanic hydrothermal vents, environments which support fragmented and unstable ecosystems, to infer the processes driving their worldwide biogeography. Besides the identification of robust provinces, the network topology allowed us to identify preferential pathways that had hitherto been overlooked. These pathways are consistent with the previously proposed hypothesis of a role of plate tectonics in the biogeographical history of hydrothermal vent communities. A possible ancestral position of the Western Pacific is also suggested for the first time. Finally, this work provides an innovative example of the potential of network tools to unravel the biogeographic history of faunal assemblages and to supply comprehensive information for the conservation and management of biodiversity.     

Genetic Markers Enhance Coronary Risk Prediction in Men: The MORGAM Prospective Cohorts

Background

More accurate coronary heart disease (CHD) prediction, specifically in middle-aged men, is needed to reduce the burden of disease more effectively. We hypothesised that a multilocus genetic risk score could refine CHD prediction beyond classic risk scores and obtain more precise risk estimates using a prospective cohort design.

Methods

Using data from nine prospective European cohorts, including 26,221 men, we selected in a case-cohort setting 4,818 healthy men at baseline, and used Cox proportional hazards models to examine associations between CHD and risk scores based on genetic variants representing 13 genomic regions. Over follow-up (range: 5–18 years), 1,736 incident CHD events occurred. Genetic risk scores were validated in men with at least 10 years of follow-up (632 cases, 1361 non-cases). Genetic risk score 1 (GRS1) combined 11 SNPs and two haplotypes, with effect estimates from previous genome-wide association studies. GRS2 combined 11 SNPs plus 4 SNPs from the haplotypes with coefficients estimated from these prospective cohorts using 10-fold cross-validation. Scores were added to a model adjusted for classic risk factors comprising the Framingham risk score and 10-year risks were derived.

Results

Both scores improved net reclassification (NRI) over the Framingham score (7.5%, p = 0.017 for GRS1, 6.5%, p = 0.044 for GRS2) but GRS2 also improved discrimination (c-index improvement 1.11%, p = 0.048). Subgroup analysis on men aged 50–59 (436 cases, 603 non-cases) improved net reclassification for GRS1 (13.8%) and GRS2 (12.5%). Net reclassification improvement remained significant for both scores when family history of CHD was added to the baseline model for this male subgroup improving prediction of early onset CHD events.

Conclusions

Genetic risk scores add precision to risk estimates for CHD and improve prediction beyond classic risk factors, particularly for middle aged men.     

Ranavirus: past, present and future

Emerging infectious diseases are a significant threat to global biodiversity. While historically overlooked, a group of iridoviruses in the genus Ranavirus has been responsible for die-offs in captive and wild amphibian, reptile and fish populations around the globe over the past two decades. In order to share contemporary information on ranaviruses and identify critical research directions, the First International Symposium on Ranaviruses was held in July 2011 in Minneapolis, MN, USA. Twenty-three scientists and veterinarians from nine countries examined the ecology and evolution of ranavirus-host interactions, potential reservoirs, transmission dynamics, as well as immunological and histopathological responses to infection. In addition, speakers discussed possible mechanisms for die-offs, and conservation strategies to control outbreaks.     

Therapeutic targeting of cancer cell cycle using proteasome inhibitors

Proteasomes are multicatalytic protease complexes in the cell, involved in the non-lysosomal recycling of intra-cellular proteins. Proteasomes play a critical role in regulation of cell division in both normal as well as cancer cells. In cancer cells this homeostatic function is deregulated leading to the hyperactivation of the proteasomes. Proteasome inhibitors (PIs) are a class of compounds, which either reversibly or irreversibly block the activity of proteasomes and induce cancer cell death. Interference of PIs with the ubiquitin proteasome pathway (UPP) involved in protein turnover in the cell leads to the accumulation of proteins engaged in cell cycle progression, which ultimately put a halt to cancer cell division and induce apoptosis. Upregulation of many tumor suppressor proteins involved in cell cycle arrest are known to play a role in PI induced cell cycle arrest in a variety of cancer cells. Although many PIs target the proteasomes, not all of them are effective in cancer therapy. Some cancers develop resistance against proteasome inhibition by possibly activating compensatory signaling pathways. However, the details of the activation of these pathways and their contribution to resistance to PI therapy remain obscure. Delineation of these pathways may help in checking resistance against PIs and deducing effective combinational approaches for improved treatment strategies. This review will discuss some of the signaling pathways related to proteasome inhibition and cell division that may help explain the basis of resistance of some cancers to proteasome inhibitors and underline the need for usage of PIs in combination with traditional chemotherapy.