The effect of enemy-release and climate conditions on invasive birds: a regional test using the rose-ringed parakeet (Psittacula krameri) as a case study

Aim Some invasive species succeed particularly well and manage to establish populations across a wide variety of regions and climatic conditions. Understanding how biotic and environmental factors facilitate their invasion success remains a challenge. Here, we assess the role of two major hypotheses explaining invasion success: (1) enemy‐release, which argues that invasive species are freed from their native predators and parasites in the new areas; and (2) climate‐matching, which argues that the climatic similarity between the exotic and native range determines the success of invasive populations. Location India, Israel and the UK. Methods We studied the reproductive success of one of the most successful avian invaders, the rose‐ringed parakeet (Psittacula krameri), in its native range (India) and in two introduced regions, varying in their climate conditions (Israel and the UK). We combined literature and field data to evaluate the role of predation pressure and climatic conditions in explaining the differences in reproductive success between the three regions. Results We found significant differences in reproductive success between regions. In accordance with the enemy‐release hypothesis, we discovered that while predation was the main factor responsible for the reduction of fecundity in India, it did not significantly affect the fecundities of parakeet populations in the two introduced regions. In accordance with the climate‐matching hypothesis, we found that in the colder temperate UK, egg infertility was high, resulting in lower fecundities. Populations in both the warmer Mediterranean climate of Israel and in the native Indian range had significantly lower egg infertility and higher fecundities than the UK populations. Main conclusions Our findings support both the enemy‐release and the climate‐matching hypotheses. While release from predators facilitates the reproductive success and therefore the invasiveness of parakeets in both the UK and in Israel, colder climate impedes reproduction and therefore the spread of parakeets in the UK.     

Predicting the potential distribution of invasive ring-necked parakeets Psittacula krameri in northern Belgium using an ecological niche modelling approach

The threat to biodiversity due to invasive alien species is considered second only to that of habitat loss. Given the large number of species that are currently invading ecosystems all over the world, we need to distinguish invaders with minor effects from those with large effects in order to prioritize management efforts. Ecological niche models can be used to predict the potential distribution of an invasive species from occurrence records and environmental data layers. We used the Ecological Niche Factor Analysis (ENFA), a presence-only predictive modelling approach, to describe the invasive ring-necked parakeets’ realized niche and to identify areas suitable for the parakeet in northern Belgium. ENFA proved to be a robust and reliable modelling technique, able to gauge the ecological requirements of an invasive species without the need to include historical information on the starting point of the invasion. ENFA shows that the parakeets tend to occupy relatively rare habitats compared to the main environmental conditions in northern Belgium, although they show some tolerance for environmental conditions inside parks and forests. The general distribution of the ring-necked parakeet is governed primarily by the amount of older forest patches, parks and built-up area in the landscape—reflecting the parakeets’ need for suitable nesting cavities and its reliance upon urban areas to forage. Our resulting habitat suitability maps show that the parakeets have ample room to further increase their range in northern Belgium. Our results indicate some concern for increased competition between parakeets and the nuthatches, native cavity nesters known to suffer from competition with parakeets, as some regions known as nuthatch strongholds are highly likely to be invaded by the parakeets.     

Salmonella Induced IL-23 and IL-1β Allow for IL-12 Production by Monocytes and M?1 through Induction of IFN-γ in CD56+ NK/NK-Like T Cells

Background

The type-1 cytokine pathway plays a pivotal role in immunity against intracellular bacterial pathogens such as Salmonellae and Mycobacteria. Bacterial stimulation of pattern recognition receptors on monocytes, macrophages and dendritic cells initiates this pathway, and results in the production of cytokines that activate lymphocytes to produce interferon (IFN)-γ. Interleukin (IL)-12 and IL-23 are thought to be the key cytokines required for initiating a type-1 cytokine immune response to Mycobacteria and Salmonellae. The relative contribution of IL-23 and IL-12 to this process is uncertain.

Methodology/Principal Findings

We show that various TLR agonists induce the production of IL-23 but not IL-12 in freshly isolated human monocytes and cultured human macrophages. In addition, type 1 pro-inflammatory macrophages (Mϕ1) differentiated in the presence of GM-CSF and infected with live Salmonella produce IL-23, IL-1β and IL-18, but not IL-12. Supernatants of Salmonella-infected Mϕ1 contained more IL-18 and IL-1β as compared with supernatants of Mϕ1 stimulated with isolated TLR agonists, and induced IFN-γ production in human CD56⁺ cells in an IL-23 and IL-1β-dependent but IL-12-independent manner. In addition, IL-23 together with IL-18 or IL-1β led to the production of GM-CSF in CD56⁺ cells. Both IFN-γ and GM-CSF enhanced IL-23 production by monocytes in response to TLR agonists, as well as induced IL-12 production.

Conclusions/Significance

The findings implicate a positive feedback loop in which IL-23 can enhance its release via induction of IFN-γ and GM-CSF. The IL-23 induced cytokines allow for the subsequent production of IL-12 and amplify the IFN-γ production in the type-1 cytokine pathway.     

Patterns of niche conservatism among non-native birds in Europe are dependent on introduction history and selection of variables

Recently, the study of niche dynamics using spatial environmental data and species occurrences has become an active field of research. Several studies report niche shifts between native and invasive populations, but it is debated whether these shifts are biologically meaningful or result from methodological artefacts. Using data on the occurrence of non-native birds in Europe, we assess the prevalence of niche shifts along a selected number of climatic variables and find that although niche differences are frequent, biological explanations are often not necessary. Niche shifts occurred more frequently along variables that were of little ecological importance in the non-native range, and about 75 % of the shifts detected do not result from range expansion into different environments but only reflect climatic conditions at introduction locations. Excluding variables exhibiting a niche shift increases the accuracy of predictions of invasion risk generated by native-range based distribution models, evidencing that selection of variables is a crucial step when studying niche changes during biological invasions.     

A genetic variant in osteoprotegerin is associated with progression of joint destruction in rheumatoid arthritis

Introduction

Progression of joint destruction in rheumatoid arthritis (RA) is partly heritably; 45 to 58% of the variance in joint destruction is estimated to be explained by genetic factors. The binding of RANKL (Receptor Activator for Nuclear Factor κ B Ligand) to RANK results in the activation of TRAF6 (tumor necrosis factor (TNF) receptor associated factor-6), and osteoclast formation ultimately leading to enhanced bone resorption. This bone resorption is inhibited by osteoprotegerin (OPG) which prevents RANKL-RANK interactions. The OPG/RANK/RANKL/TRAF6 pathway plays an important role in bone remodeling. Therefore, we investigated whether genetic variants in OPG, RANK, RANKL and TRAF6 are associated with the rate of joint destruction in RA.

Methods

1,418 patients with 4,885 X-rays of hands and feet derived from four independent data-sets were studied. In each data-set the relative increase of the progression rate per year in the presence of a genotype was assessed. First, explorative analyses were performed on 600 RA-patients from Leiden. 109 SNPs, tagging OPG, RANK, RANKL and TRAF6, were tested. Single nucleotide polymorphisms (SNPs) significantly associated in phase-1 were genotyped in data-sets from Groningen (Netherlands), Sheffield (United Kingdom) and Lund (Switzerland). Data were summarized in an inverse weighted variance meta-analysis. Bonferonni correction for multiple testing was applied.

Results

We found that 33 SNPs were significantly associated with the rate of joint destruction in phase-1. In phase-2, six SNPs in OPG and four SNPs in RANK were associated with progression of joint destruction with P-value <0.05. In the meta-analyses of all four data-sets, RA-patients with the minor allele of OPG-rs1485305 expressed higher rates of joint destruction compared to patients without these risk variants (P = 2.35x10⁻⁴). This variant was also significant after Bonferroni correction.

Conclusions

These results indicate that a genetic variant in OPG is associated with a more severe rate of joint destruction in RA.     

Myocardial Infarction-induced N-terminal Fragment of Cardiac Myosin-binding Protein C (cMyBP-C) Impairs Myofilament Function in Human Myocardium

Myocardial infarction (MI) is associated with depressed cardiac contractile function and progression to heart failure. Cardiac myosin-binding protein C, a cardiac-specific myofilament protein, is proteolyzed post-MI in humans, which results in an N-terminal fragment, C0-C1f. The presence of C0-C1f in cultured cardiomyocytes results in decreased Ca²⁺ transients and cell shortening, abnormalities sufficient for the induction of heart failure in a mouse model. However, the underlying mechanisms remain unclear. Here, we investigate the association between C0-C1f and altered contractility in human cardiac myofilaments in vitro. To accomplish this, we generated recombinant human C0-C1f (hC0C1f) and incorporated it into permeabilized human left ventricular myocardium. Mechanical properties were studied at short (2 μm) and long (2.3 μm) sarcomere length (SL). Our data demonstrate that the presence of hC0C1f in the sarcomere had the greatest effect at short, but not long, SL, decreasing maximal force and myofilament Ca²⁺ sensitivity. Moreover, hC0C1f led to increased cooperative activation, cross-bridge cycling kinetics, and tension cost, with greater effects at short SL. We further established that the effects of hC0C1f occur through direct interaction with actin and α-tropomyosin. Our data demonstrate that the presence of hC0C1f in the sarcomere is sufficient to induce depressed myofilament function and Ca²⁺ sensitivity in otherwise healthy human donor myocardium. Decreased cardiac function post-MI may result, in part, from the ability of hC0C1f to bind actin and α-tropomyosin, suggesting that cleaved C0-C1f could act as a poison polypeptide and disrupt the interaction of native cardiac myosin-binding protein C with the thin filament.     

Visualization of ribosomal DNA loci in spore interphasic nuclei of glomalean fungi by fluorescence in situ hybridization

 Fluorescence in situ hybridization (FISH) was applied to interphasic nuclei isolated from spores of four species of AM fungi : Scutellospora castanea, Glomus mosseae, Glomus intraradices and Gigaspora rosea. Ribosomal DNA loci were visualized using digoxigenin-labeled 25 S rDNA probes obtained by nested PCR. Several hybridization sites were detected per nucleus and an internuclear variability was observed in the number of loci. This is the first report of successful application of FISH to analyse the genomes of glomalean fungi. Accepted: 16 September 1998