Ensemble modelling of species distribution: the effects of geographical and environmental ranges

The aim of this study was to analyse the effects of species geographical and environmental ranges on the predictive performances of species distribution models (SDMs). We explored the usefulness of ensemble modelling approaches and tested whether species attributes influenced the outcomes of such approaches. Eight SDMs were used to model the current distribution of 35 fish species at 1110 stream sections in France. We first quantified the consensus among the resulting set of predictions for each fish species. Next, we created an average model by taking the average of the individual model predictions and tested whether the average model improved the predictive performances of single SDMs. Lastly, we described the ranges of fish species along four gradients: latitudinal, thermal, stream gradient (i.e. upstream‐downstream) and elevation. After accounting for the effects of phylogenetic relatedness and species prevalence, these four species attributes were related to the observed variations in both consensus among SDMs and predictive performances by using generalized estimation equations. Our results highlight the usefulness of ensemble approaches for identifying geographical areas of agreement among predictions. Although the geographical extent of species had no effect on the performances of SDMs, we demonstrated that more consensual and accurate predictions were obtained for species with low thermal and elevation ranges, validating the hypothesis that specialist species yield models with higher accuracy than generalist ones. We emphasized that significant improvements in the accuracy of SDMs can be achieved by using an average model. Furthermore, these improvements were higher for species with smaller ranges along the four gradients studied. The geographical extent and ranges of species along environmental gradients provide promising insights into our understanding of uncertainties in species distribution modelling.     

Impact of agricultural land use on aquatic insect assemblages in the Garonne river catchment (SW France)

The impact of agricultural land use on the composition and structure of aquatic insect assemblages (i.e., taxa of Ephemeroptera, Plecoptera, Trichoptera, and Coleoptera (EPTC)) was investigated in tributary streams of the Garonne river basin, southern France. The self-organizing map (SOM) method was applied to compare both instream environmental conditions and EPTC assemblages between forest and agricultural streams. According to the SOM model, the study sites were classified into three main clusters corresponding to distinct EPTC assemblages. The SOM cluster associated with most of the agricultural sites had lower EPTC species richness and diversity. This cluster was also characterized by high levels of total dissolved solids, nitrate (NO₃), and chemical oxygen demand. Overall, our study shows that agricultural streams when compared with forest streams had lower biological integrity. In accordance with the European Water Framework Directive, our results indicate that the sites most impacted by agricultural land use should be restored and that the least-impacted forest sites could serve as reference conditions.     

Why do parasitized hosts look different? Resolving the “chicken-egg” dilemma

Phenotypic differences between infected and non-infected hosts are often assumed to be the consequence of parasite infection. However, pre-existing differences in hosts’ phenotypes may promote differential susceptibility to infection. The phenotypic variability observed within the host population may therefore be a cause rather than a consequence of infection. In this study, we aimed at disentangling the causes and the consequences of parasite infection by calculating the value of a phenotypic trait (i.e., the growth rate) of the hosts both before and after infection occurred. That procedure was applied to two natural systems of host–parasite interactions. In the first system, the infection level of an ectoparasite (Tracheliastes polycolpus) decreases the growth rate of its fish host (the rostrum dace, Leuciscus leuciscus). Reciprocally, this same phenotypic trait before infection modulated the future level of host sensitivity to the direct pathogenic effect of the parasite, namely the level of fin degradation. In the second model, causes and consequences linked the growth rate of the fish host (the rainbow smelt, Osmerus mordax) and the level of endoparasite infection (Proteocephalus tetrastomus). Indeed, the host’s growth rate before infection determined the number of parasites later in life, and the parasite biovolume then decreased the host’s growth rate of heavily infected hosts. We demonstrated that reciprocal effects between host phenotypes and parasite infection can occur simultaneously in the wild, and that the observed variation in the host phenotype population was not necessarily a consequence of parasite infection. Disentangling the causality of host–parasite interactions should contribute substantially to evaluating the role of parasites in ecological and evolutionary processes. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users.     

Temporal Patterns of Larval Fish Occurrence in a Large Subtropical River

Knowledge of temporal patterns of larval fish occurrence is limited in south China, despite its ecological importance. This research examines the annual and seasonal patterns of fish larval presence in the large subtropical Pearl River. Data is based on samples collected every two days, from 2006 to 2013. In total, 45 taxa representing 13 families and eight orders were sampled. The dominant larval family was Cyprinidae, accounting for 27 taxa. Squaliobarbus curriculus was the most abundant species, followed by Megalobrama terminalis, Xenocypris davidi, Cirrhinus molitorella, Hemiculter leuscisculus and Squalidus argentatus. Fish larvae abundances varied significantly throughout the seasons (multivariate analyses: Cluster, SIMPROF and ANOSIM). The greatest numbers occurred between May and September, peaking from June through August, which corresponds to the reproductive season. In this study, redundancy analysis was used to describe the relationship between fish larval abundance and associated environmental factors. Mean water temperature, river discharge, atmospheric pressure, maximum temperature and precipitation play important roles in larval occurrence patterns. According to seasonal variations, fish larvae occurrence is mainly affected by water temperature. It was also noted that the occurrence of Salanx reevesii and Cyprinus carpio larvae is associated with higher dissolved oxygen (DO) concentrations, higher atmospheric pressure and lower water temperatures which occur in the spring. On the other hand, M. terminalis, X. davidi, and C. molitorella are associated with high precipitation, high river discharge, low atmospheric pressure and low DO concentrations which featured during the summer months. S. curriculus also peaks in the summer and is associated with peak water temperatures and minimum NH₃–N concentrations. Rhinogobius giurinus occur when higher atmospheric pressure, lower precipitation and lower river discharges occur in the autumn. Dominant fish species stagger their spawning period to avoid intraspecific competition for food resources during early life stages; a coexistence strategy to some extent. This research outlines the environmental requirements for successful spawning for different fish species. Understanding processes such as those outlined in this research paper is the basis of conservation of fish community diversity which is a critical resource to a successful sustainable fishery in the Pearl River.     

Novel targets for Huntington's disease in an mTOR-independent autophagy pathway

Autophagy is a major clearance route for intracellular aggregate-prone proteins causing diseases such as Huntington's disease. Autophagy induction with the mTOR inhibitor rapamycin accelerates clearance of these toxic substrates. As rapamycin has nontrivial side effects, we screened FDA-approved drugs to identify new autophagy-inducing pathways. We found that L-type Ca2+ channel antagonists, the K+ATP channel opener minoxidil, and the G(i) signaling activator clonidine induce autophagy. These drugs revealed a cyclical mTOR-independent pathway regulating autophagy, in which cAMP regulates IP3 levels, influencing calpain activity, which completes the cycle by cleaving and activating G(s)alpha, which regulates cAMP levels. This pathway has numerous potential points where autophagy can be induced, and we provide proof of principle for therapeutic relevance in Huntington's disease using mammalian cell, fly and zebrafish models. Our data also suggest that insults that elevate intracytosolic Ca2+ (like excitotoxicity) inhibit autophagy, thus retarding clearance of aggregate-prone proteins.     

Huntington's disease: degradation of mutant huntingtin by autophagy

Autophagy is a nonspecific bulk degradation pathway for long-lived cytoplasmic proteins, protein complexes, or damaged organelles. This process is also a major degradation pathway for many aggregate-prone, disease-causing proteins associated with neurodegenerative disorders, such as mutant huntingtin in Huntington's disease. In this review, we discuss factors regulating the degradation of mutant huntingtin by autophagy. We also report the growing list of new drugs/pathways that upregulate autophagy to enhance the clearance of this mutant protein, as autophagy upregulation may be a tractable strategy for the treatment of Huntington's disease.     

Small molecule enhancers of autophagy for neurodegenerative diseases

Neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, prion diseases and polyglutamine disorders, including Huntington's disease and various spinocerebellar ataxias, are associated with the formation of protein aggregates. These aggregates and/or their precursors are thought to be toxic disease-causing species. Autophagy is a major degradation pathway for intracytosolic aggregate-prone proteins, including those associated with neurodegeneration. It is a constitutive self-degradative process involved both in the basal turnover of cellular components and in response to nutrient starvation in eukaryotes. Enhancing autophagy may be a possible therapeutic strategy for neurodegenerative disorders where the mutant proteins are autophagy substrates. In cell and animal models, chemical induction of autophagy protects against the toxic insults of these mutant aggregate-prone proteins by enhancing their clearance. We will discuss various autophagy-inducing small molecules that have emerged in the past few years that may be leads towards the treatment of such devastating diseases.     

Geography and host specificity: two forces behind the genetic structure of the freshwater fish parasite Ligula intestinalis (Cestoda: Diphyllobothriidae)

Parasite species with global distributions and complex life cycles offer a rare opportunity to study alternative mechanisms of speciation and evolution in a single model. Here, genealogy and genetic structure, with respect to geography and fish host preference, have been analyzed for Ligula intestinalis, a tapeworm affecting freshwater fish. The data analyzed consisted of 109 tapeworms sampled from 13 fish host species in 18 different localities on a macrogeographic scale. Two mitochondrial genes, cytochrome oxidase subunit I and cytochrome B, and the nuclear sequence of intergenic transcribed spacer 2 (ITS2) were used for the genetic reconstruction. Different evolutionary patterns were found at the local and at the global geographic scales. On a local scale, the flat genetic structure was mainly attributed to contiguous range expansion. Migrating birds are the most likely cause of the homogenisation of the whole population, preventing the creation of significant genetic barriers. By contrast, on a global scale, genetically distant and well-separated clusters are present in different geographic areas. Reproductive isolation was found even between clades living in sympatry and infecting the same definitive host, suggesting the existence of efficient biologically determined genetic barriers, and thus possibly separate species. Although the ITS2 sequences were found to display considerable intragenomic variability, their relationships were generally in good agreement with the topology derived from mitochondrial genes.     

Impaired autophagy in Lafora disease

Lafora disease (LD) is a progressive, lethal, autosomal recessive, neurodegenerative disorder that manifests with myoclonus epilepsy. LD is characterized by the presence of intracellular inclusion bodies called Lafora bodies (LB), in brain, spinal cord and other tissues. More than 50 percent of LD is caused by mutations in EPM2A that encodes laforin. Here we review our recent findings that revealed that laforin regulates autophagy. We consider how autophagy compromise may predispose to LB formation and neurodegeneration in LD, and discuss future investigations suggested by our data.Key words: autophagy, glycogen metabolism, Lafora disease, laforin, malin, neurodegeneration