Pathogenesis of acute viral disease induced in fish by carp interstitial nephritis and gill necrosis virus

A lethal disease of koi and common carp (species Cyprinus carpio) has afflicted many fish farms worldwide since 1998, causing severe financial losses. Morbidity and mortality are restricted to common carp and koi and appear in spring and autumn, when water temperatures are 18 to 28 degrees C. We have isolated the virus causing the disease from sick fish, propagated it in koi fin cell culture, and shown that virus from a single clone causes lethal disease in carp and koi upon infection. Intraperitoneal virus injection or bathing the fish in virus-containing water kills 85 to 100% of the fish within 7 to 21 days. This virus is similar to the previously reported koi herpesvirus; however, it has characteristics inconsistent with the herpesvirus family, and thus we have called it carp interstitial nephritis and gill necrosis virus. We examined the pathobiology of this disease in carp by using immunohistochemistry and PCR. We found large amounts of the virus in the kidneys of sick fish and smaller amounts in liver and brain. A rapid increase in the viral load in the kidneys was detected by using both immunofluorescence and semiquantitative PCR. Histological analyses of fish at various times after infection revealed signs of interstitial nephritis as early as 2 days postinfection, which increased in severity up to 10 days postinfection. There was severe gill disease evidenced by loss of villi with accompanying inflammation in the gill rakers. Minimal focal inflammation was noted in livers and brains. This report describes the etiology and pathology of a recently described viral agent in fish.     

Conceptual Modeling of mRNA Decay Provokes New Hypotheses

Biologists are required to integrate large amounts of data to construct a working model of the system under investigation. This model is often informal and stored mentally or textually, making it prone to contain undetected inconsistencies, inaccuracies, or even contradictions, not much less than a representation in free natural language. Using Object-Process Methodology (OPM), a formal yet visual and humanly accessible conceptual modeling language, we have created an executable working model of the mRNA decay process in Saccharomyces cerevisiae, as well as the import of its components to the nucleus following mRNA decay. We show how our model, which incorporates knowledge from 43 articles, can reproduce outcomes that match the experimental findings, evaluate hypotheses, and predict new possible outcomes. Moreover, we were able to analyze the effects of the mRNA decay model perturbations related to gene and interaction deletions, and predict the nuclear import of certain decay factors, which we then verified experimentally. In particular, we verified experimentally the hypothesis that Rpb4p, Lsm1p, and Pan2p remain bound to the RNA 3′-untralslated region during the entire process of the 5′ to 3′ degradation of the RNA open reading frame. The model has also highlighted erroneous hypotheses that indeed were not in line with the experimental outcomes. Beyond the scientific value of these specific findings, this work demonstrates the value of the conceptual model as an in silico vehicle for hypotheses generation and testing, which can reinforce, and often even replace, risky, costlier wet lab experiments.     

Analysis of climate paths reveals potential limitations on species range shifts

Forecasts of species endangerment under climate change usually ignore the processes by which species ranges shift. By analysing the 'climate paths' that range shifts might follow, and two key range-shift processes--dispersal and population persistence--we show that short-term climatic and population characteristics have dramatic effects on range-shift forecasts. By employing this approach with 15 amphibian species in the western USA, we make unexpected predictions. First, inter-decadal variability in climate change can prevent range shifts by causing gaps in climate paths, even in the absence of geographic barriers. Second, the hitherto unappreciated trait of persistence during unfavourable climatic conditions is critical to species range shifts. Third, climatic fluctuations and low persistence could lead to endangerment even if the future potential range size is large. These considerations may render habitat corridors ineffectual for some species, and conservationists may need to consider managed relocation and augmentation of in situ populations.     

Transition of endothelium to cartilage and bone

Mesenchymal stromal cells (MSCs) are capable of differentiating into bone-forming osteoblasts. A recent Nature Medicine study (Medici et al., 2010) shows that the mislocalized bone in the human disease fibrodisplasia ossificans progressiva (FOP) originates from vascular endothelium that gives rise to MSCs.     

Erratum: TMOF‐like factor controls the biosynthesis of serine proteases in the larval gut of Heliothis virescens

In our recently published paper, we the authors have found that in Table 3 there was a mistake in the statistical analysis of injected and control animals; they are not statistically different. Because of this faulty analysis, we initially did not find it necessary to include the 72 hour results that are highly statistically different. The amended Table 3 and the original article’s title page appear below.     

Effects of exotic species on evolutionary diversification

Exotic species invasions create almost ideal conditions for promoting evolutionary diversification: establishment of allopatric populations in new environmental conditions; altered ecological opportunities for native species; and new opportunities for hybridization between previously allopatric taxa. Here, we review recent studies of the evolutionary consequences of species invasions, revealing abundant and widespread examples of exotic species promoting evolutionary diversification via increased genetic differentiation among populations of both exotic and native species and the creation of new hybrid lineages. Our review indicates that, although the well-documented reductions to biodiversity caused by exotic species might outweigh the increases resulting from diversification, a complete understanding of the net effects of exotic species on biodiversity in the long term will require consideration of both.     

Sugar-regulated susceptibility of tomato fruit to Colletotrichum and Penicillium requires differential mechanisms of pathogenicity and fruit responses

Colletotrichum gloeosporioides and Penicillium expansum cause postharvest diseases in tropical and deciduous fruit. During colonization, C. gloeosporioides and P. expansum secrete ammonia in hosts with low sugar content (LowSC) and gluconic acid in hosts with high sugar content (HighSC), respectively, as a mechanism to modulate enhanced pathogenicity. We studied the pathogens interactions with tomato lines of similar genetic background but differing in their sugar content. Colletotrichum gloeosporioides showed enhanced colonization of the LowSC line with differential expression response of 15% of its genes including enhanced relative expression of glycosyl hydrolases, glucanase and MFS-transporter genes. Enhanced colonization of P. expansum occurred in the HighSC line, accompanied by an increase in carbohydrate metabolic processes mainly phosphoenolpyruvate carboxykinase, and only 4% of differentially expressed genes. Gene response of the two host lines strongly differed depending on the sugar level. Limited colonization of HighSC line by C. gloeosporioides was accompanied by a marked alteration of gene expression compared the LowSC response to the same pathogen; while colonization by P. expansum resulted in a similar response of the two different hosts. We suggest that this differential pattern of fungal/host responses may be the basis for the differential of host range of both pathogens in nature.