Evaluating nuclear protein-coding genes for phylogenetic utility in beetles

Although nuclear protein-coding genes have proven broadly useful for phylogenetic inference, relatively few such genes are regularly employed in studies of Coleoptera, the most diverse insect order. We increase the number of loci available for beetle systematics by developing protocols for three genes previously unused in beetles (alpha-spectrin, RNA polymerase II and topoisomerase I) and by refining protocols for five genes already in use (arginine kinase, CAD, enolase, PEPCK and wingless). We evaluate the phylogenetic performance of each gene in a Bayesian framework against a presumably known test phylogeny. The test phylogeny covers 31 beetle specimens and two outgroup taxa of varying age, including three of the four extant beetle suborders and a denser sampling in Adephaga and in the carabid genus Bembidion. All eight genes perform well for Cenozoic divergences and accurately separate closely related species within Bembidion, but individual genes differ markedly in accuracy over the older Mesozoic and Permian divergences. The concatenated data reconstruct the test phylogeny with high support in both Bayesian and parsimony analyses, indicating that combining data from multiple nuclear loci will be a fruitful approach for assembling the beetle tree of life.     

Diaphragm adaptations in patients with COPD

Inspiratory muscle weakness in patients with COPD is of major clinical relevance. For instance, maximum inspiratory pressure generation is an independent determinant of survival in severe COPD. Traditionally, inspiratory muscle weakness has been ascribed to hyperinflation-induced diaphragm shortening. However, more recently, invasive evaluation of diaphragm contractile function, structure, and biochemistry demonstrated that cellular and molecular alterations occur, of which several can be considered pathologic of nature. Whereas the fiber type shift towards oxidative type I fibers in COPD diaphragm is regarded beneficial, rendering the overloaded diaphragm more resistant to fatigue, the reduction of diaphragm fiber force generation in vitro likely contributes to diaphragm weakness. The reduced diaphragm force generation at single fiber level is associated with loss of myosin content in these fibers. Moreover, the diaphragm in COPD is exposed to oxidative stress and sarcomeric injury. This review postulates that the oxidative stress and sarcomeric injury activate proteolytic machinery, leading to contractile protein wasting and, consequently, loss of force generating capacity of diaphragm fibers in patients with COPD. Interestingly, several of these presumed pathologic alterations are already present early in the course of the disease (GOLD I/II), although these patients appear not limited in their daily life activities. Treatment of diaphragm dysfunction in COPD is complex since its etiology is unclear, but recent findings indicate the ubiquitin-proteasome pathway as a prime target to attenuate diaphragm wasting in COPD.     

Association between the risk of coronary artery disease in South Asians and a deletion polymorphism in glutathione S-transferase M1.

South Asians living in Western societies show a greater risk of coronary artery disease (CAD) than the indigenous Caucasian population, probably related to the change to a Westernised lifestyle and an associated genetic susceptibility. Modulation of DNA damage and mutation caused by polymorphisms in detoxification enzymes, including the glutathione S-transferases (GSTs), is a well-established risk factor for tobacco-related carcinogenesis, and a similar change in cellular damage may be involved in the risk of vascular disease associated with tobacco smoking. In this study we examined whether polymorphisms in GST genes influence the risk of CAD in a case-control group of South Asians, following our recent observation of such an association in Caucasians from the same region of the UK. Blood was obtained from 170 patients of South Asian origin admitted for angiographic investigation of chest pain and from 203 controls. Patients were subdivided into those with and without previous acute myocardial infarction (AMI), and DNA was analysed for deletions in the GSTM1 and GSTT1 genes. An association was found between the prevalence of the GSTM1 null genotype and the risk of developing CAD in this study population. The frequency of the null genotype was 52.7% in healthy controls and 41.2% in patients (odds ratio [OR] 0.63, 95% confidence interval [95% CI] 0.42-0.95, p = 0.029). The effect was similar in subjects with or without a prior history of AMI. The association was also independent of smoking history, with both non-smokers and smokers showing a similar pattern of genotype distribution, the frequency of the null genotype being 51.2% in controls versus 37.0% in patients in 'never' smokers (OR 0.56, 95% CI 0.33-0.94, p = 0.037) and 60.0% in controls versus 46.2% in patients in 'ever' smokers (OR 0.57, 95% CI 0.25-1.28, p = 0.223). The association remained after adjusting for age, sex, body mass index and the presence or absence of stenosis. No significant associations were observed between the GSTT1 genotype and cardiovascular disease (chi(2) test, p > 0.1). The results of this study indicate that the GSTM1 null genotype is protective against both CAD and AMI. However, further study is required in order to elucidate the, as yet unexplained, mechanisms underlying this association.     

DNA damage levels are raised in Barrett's oesophageal mucosa relative to the squamous epithelium of the oesophagus.

Barrett's oesophagus (BE) is a pre-malignant metaplastic tissue predisposing to oesophageal adenocarcinoma (EC), and gastro-oesophageal reflux is a risk factor for both conditions. Reflux of acid and bile can cause mucosal injury and initiate chronic inflammation. These processes can induce DNA damage, possibly via an oxidative stress mechanism, thus increasing the likelihood of progression from Barrett's metaplasia to dysplasia and finally carcinoma. The comet assay was optimized for the detection of DNA damage (strand breaks and alkali-labile sites) in oesophageal biopsies, including incorporation of the DNA repair enzyme Fapy-DNA glycosylase (Fpg). Fpg allows the detection of 8-hydroxy-2-deoxyguanosine (8-OHdG) sites, a known pro-mutagenic DNA lesion. BE patients were recruited from BE surveillance clinics and oesophageal biopsies collected at endoscopy. Comet analysis revealed significantly increased (p < 0.001) DNA damage in Barrett's epithelium compared with matched squamous epithelium, with median % tail DNA values of 25.1% (first to third quartile 21.7-29.6%) and 18.6% (first to third quartile 16.9-21.4%), respectively. The median % tail DNA was up to 70% higher in the matched BE tissue compared with squamous epithelium from the same patient. Fpg sensitive sites were demonstrated in both tissue types at similar levels. The raised level of DNA damage in the premalignant BE may contribute to the accumulation of genetic alterations occurring during progression to EC. Understanding these underlying mechanisms provides a basis for cancer prevention strategies in BE patients.     

European map of alien plant invasions based on the quantitative assessment across habitats

Aim Recent studies using vegetation plots have demonstrated that habitat type is a good predictor of the level of plant invasion, expressed as the proportion of alien to all species. At local scale, habitat types explain the level of invasion much better than alien propagule pressure. Moreover, it has been shown that patterns of habitat invasion are consistent among European regions with contrasting climates, biogeography, history and socioeconomic background. Here we use these findings as a basis for mapping the level of plant invasion in Europe. Location European Union and some adjacent countries. Methods We used 52,480 vegetation plots from Catalonia (NE Spain), Czech Republic and Great Britain to quantify the levels of invasion by neophytes (alien plant species introduced after ad 1500) in 33 habitat types. Then we estimated the proportion of each of these habitat types in CORINE land‐cover classes and calculated the level of invasion for each class. We projected the levels of invasion on the CORINE land‐cover map of Europe, extrapolating Catalonian data to the Mediterranean bioregion, Czech data to the Continental bioregion, British data to the British Isles and combined Czech–British data to the Atlantic and Boreal bioregions. Results The highest levels of invasion were predicted for agricultural, urban and industrial land‐cover classes, low levels for natural and semi‐natural grasslands and most woodlands, and the lowest levels for sclerophyllous vegetation, heathlands and peatlands. The resulting map of the level of invasion reflected the distribution of these land‐cover classes across Europe. Main conclusions High level of invasion is predicted in lowland areas of the temperate zone of western and central Europe and low level in the boreal zone and mountain regions across the continent. Low level of invasion is also predicted in the Mediterranean region except its coastline, river corridors and areas with irrigated agricultural land.     

Nix is a selective autophagy receptor for mitochondrial clearance

Autophagy is the cellular homeostatic pathway that delivers large cytosolic materials for degradation in the lysosome. Recent evidence indicates that autophagy mediates selective removal of protein aggregates, organelles and microbes in cells. Yet, the specificity in targeting a particular substrate to the autophagy pathway remains poorly understood. Here, we show that the mitochondrial protein Nix is a selective autophagy receptor by binding to LC3/GABARAP proteins, ubiquitin‐like modifiers that are required for the growth of autophagosomal membranes. In cultured cells, Nix recruits GABARAP‐L1 to damaged mitochondria through its amino‐terminal LC3‐interacting region. Furthermore, ablation of the Nix:LC3/GABARAP interaction retards mitochondrial clearance in maturing murine reticulocytes. Thus, Nix functions as an autophagy receptor, which mediates mitochondrial clearance after mitochondrial damage and during erythrocyte differentiation.     

The Nonstructural Proteins of Nipah Virus Play a Key Role in Pathogenicity in Experimentally Infected Animals

Nipah virus (NiV) P gene encodes P protein and three accessory proteins (V, C and W). It has been reported that all four P gene products have IFN antagonist activity when the proteins were transiently expressed. However, the role of those accessory proteins in natural infection with NiV remains unknown. We generated recombinant NiVs lacking V, C or W protein, rNiV(V−), rNiV(C−), and rNiV(W−), respectively, to analyze the functions of these proteins in infected cells and the implications in in vivo pathogenicity. All the recombinants grew well in cell culture, although the maximum titers of rNiV(V−) and rNiV(C−) were lower than the other recombinants. The rNiV(V−), rNiV(C−) and rNiV(W−) suppressed the IFN response as well as the parental rNiV, thereby indicating that the lack of each accessory protein does not significantly affect the inhibition of IFN signaling in infected cells. In experimentally infected golden hamsters, rNiV(V−) and rNiV(C−) but not the rNiV(W−) virus showed a significant reduction in virulence. These results suggest that V and C proteins play key roles in NiV pathogenicity, and the roles are independent of their IFN-antagonist activity. This is the first report that identifies the molecular determinants of NiV in pathogenicity in vivo.     

Pego do Diabo (Loures,Portugal): Dating the Emergence of Anatomical Modernity in Westernmost Eurasia

Background

Neandertals and the Middle Paleolithic persisted in the Iberian Peninsula south of the Ebro drainage system for several millennia beyond their assimilation/replacement elsewhere in Europe. As only modern humans are associated with the later stages of the Aurignacian, the duration of this persistence pattern can be assessed via the dating of diagnostic occurrences of such stages.

Methodology/Principal Findings

Using AMS radiocarbon and advanced pretreatment techniques, we dated a set of stratigraphically associated faunal samples from an Aurignacian III–IV context excavated at the Portuguese cave site of Pego do Diabo. Our results establish a secure terminus ante quem of ca.34,500 calendar years ago for the assimilation/replacement process in westernmost Eurasia. Combined with the chronology of the regional Late Mousterian and with less precise dating evidence for the Aurignacian II, they place the denouement of that process in the 37th millennium before present.

Conclusions/Significance

These findings have implications for the understanding of the emergence of anatomical modernity in the Old World as a whole, support explanations of the archaic features of the Lagar Velho child''s anatomy that invoke evolutionarily significant Neandertal/modern admixture at the time of contact, and counter suggestions that Neandertals could have survived in southwest Iberia until as late as the Last Glacial Maximum.     

Sugar enrichment provides evidence for a role of nitrogen fixation in coral bleaching

The disruption of the coral–algae symbiosis (coral bleaching) due to rising sea surface temperatures has become an unprecedented global threat to coral reefs. Despite decades of research, our ability to manage mass bleaching events remains hampered by an incomplete mechanistic understanding of the processes involved. In this study, we induced a coral bleaching phenotype in the absence of heat and light stress by adding sugars. The sugar addition resulted in coral symbiotic breakdown accompanied by a fourfold increase of coral‐associated microbial nitrogen fixation. Concomitantly, increased N:P ratios by the coral host and algal symbionts suggest excess availability of nitrogen and a disruption of the nitrogen limitation within the coral holobiont. As nitrogen fixation is similarly stimulated in ocean warming scenarios, here we propose a refined coral bleaching model integrating the cascading effects of stimulated microbial nitrogen fixation. This model highlights the putative role of nitrogen‐fixing microbes in coral holobiont functioning and breakdown.     

Signalling of information that is neither cryptic nor private

It is commonly assumed that in order for animal signals to be advantageous, the information being signalled could not have been obtained otherwise, and is therefore ‘cryptic’ or ‘private’. Here, we suggest a scenario in which individuals can gain an advantage by signalling ‘public’ information that is neither cryptic nor private. In that scenario, signalling increases the efficiency with which that ‘public’ information is transmitted. We formalize our idea with a game in which offspring can signal their condition to their parents. Specifically, we consider a resource‐strapped parent who can only invest in one of its two offspring, and we allow offspring the chance to influence parental investment through a signal. A parent in the game seeks to invest in the higher‐quality offspring, which it could identify either through a publicly available cue, such as body size, or by relying on a signal provided by the offspring. We find that if the signal can convey information about offspring quality more efficiently than cues, then signalling of condition between offspring and parents can be favoured by selection, even though parents could potentially have acquired the same information from the cue. Our results suggest that the biological function of signals may be broader than currently considered, and provide a scenario where low cost signalling can be favoured. More generally, efficiency benefits could explain signalling across a range of biological and economic scenarios.