Can size distributions of European lake fish communities be predicted by trophic positions of their fish species?

An organism''s body size plays an important role in ecological interactions such as predator–prey relationships. As predators are typically larger than their prey, this often leads to a strong positive relationship between body size and trophic position in aquatic ecosystems. The distribution of body sizes in a community can thus be an indicator of the strengths of predator–prey interactions. The aim of this study was to gain more insight into the relationship between fish body size distribution and trophic position in a wide range of European lakes. We used quantile regression to examine the relationship between fish species'' trophic position and their log‐transformed maximum body mass for 48 fish species found in 235 European lakes. Subsequently, we examined whether the slopes of the continuous community size distributions, estimated by maximum likelihood, were predicted by trophic position, predator–prey mass ratio (PPMR), or abundance (number per unit effort) of fish communities in these lakes. We found a positive linear relationship between species'' maximum body mass and average trophic position in fishes only for the 75% quantile, contrasting our expectation that species'' trophic position systematically increases with maximum body mass for fish species in European lakes. Consequently, the size spectrum slope was not related to the average community trophic position, but there were negative effects of community PPMR and total fish abundance on the size spectrum slope. We conclude that predator–prey interactions likely do not contribute strongly to shaping community size distributions in these lakes.     

ER-lysosome lipid transfer protein VPS13C/PARK23 prevents aberrant mtDNA-dependent STING signaling

Mutations in VPS13C cause early-onset, autosomal recessive Parkinson’s disease (PD). We have established that VPS13C encodes a lipid transfer protein localized to contact sites between the ER and late endosomes/lysosomes. In the current study, we demonstrate that depleting VPS13C in HeLa cells causes an accumulation of lysosomes with an altered lipid profile, including an accumulation of di-22:6-BMP, a biomarker of the PD-associated leucine-rich repeat kinase 2 (LRRK2) G2019S mutation. In addition, the DNA-sensing cGAS-STING pathway, which was recently implicated in PD pathogenesis, is activated in these cells. This activation results from a combination of elevated mitochondrial DNA in the cytosol and a defect in the degradation of activated STING, a lysosome-dependent process. These results suggest a link between ER-lysosome lipid transfer and innate immune activation in a model human cell line and place VPS13C in pathways relevant to PD pathogenesis.     

Soil organic matter molecular composition and state of decomposition in three locations of the European Arctic

Increased mineralization of the organic matter (OM) stored in permafrost is expected to constitute the largest additional global warming potential from terrestrial ecosystems exposed to a warmer climate. Chemical composition of permafrost OM is thought to be a key factor controlling the sensitivity of decomposition to warming. Our objective was to characterise OM from permafrost soils of the European Arctic: two mineral soils—Adventdalen, Svalbard, Norway and Vorkuta, northwest Russia—and a “palsa” (ice-cored peat mound patterning in heterogeneous permafrost landscapes) soil in Neiden, northern Norway, in terms of molecular composition and state of decomposition. At all sites, the OM stored in the permafrost was at an advanced stage of decomposition, although somewhat less so in the palsa peat. By comparing permafrost and active layers, we found no consistent effect of depth or permafrost on soil organic matter (SOM) chemistry across sites. The permafrost-affected palsa peat displayed better preservation of plant material in the deeper layer, as indicated by increasing contribution of lignin carbon to total carbon with depth, associated to decreasing acid (Ac) to aldehyde (Al) ratio of the syringyl (S) and vanillyl (V) units, and increasing S/V and contribution of plant-derived sugars. By contrast, in Adventdalen, the Ac/Al ratio of lignin and the Alkyl C to O-alkyl C ratio in the NMR spectra increased with depth, which suggests less oxidized SOM in the active layer compared to the permafrost layer. In Vorkuta, SOM characteristics in the permafrost profile did not change substantially with depth, probably due to mixing of soil layers by cryoturbation. The composition and state of decomposition of SOM appeared to be site-specific, in particular bound to the prevailing organic or mineral nature of soil when attempting to predict the SOM proneness to degradation. The occurrence of processes such as palsa formation in organic soils and cryoturbation should be considered when up-scaling and predicting the responses of OM to climate change in arctic soils.     

Nuclear localization of TRK-A in liver cells

The liver represents a site of expression of neurotrophins and their receptors. We have characterized the expression and intracellular localization of the nerve growth factor (NGF) receptor, Trk-A, in liver cells in vivo and in vitro. In both normal and fibrotic liver tissue, Trk-A immunostaining was present in different cell types, including parenchymal cells and cells of the inflammatory infiltrate. In hepatocytes and activated stellate cells (HSC), Trk-A showed a predominant nuclear localization, both in the presence and absence of injury. In cultured HSC, Trk-A was found to be functional, because exposure of the cells to recombinant NGF resulted in stimulation of cell migration and activation of intracellular signaling pathways, including Ras-ERK and PI3K/Akt. Remarkably, in cultured HSC, Trk-A staining was found constitutively in the nucleus. In these cells, Trk-A could be stained only by antibodies directed against the intracellular domain but not by those recognizing the extracellular portion of Trk-A suggesting that the intracellular portion of the receptor is the major determinant of nuclear Trk-A staining. In contrast to HSC, freshly isolated hepatocytes did not show any nuclear localization of the intracellular portion of Trk-A. In pheocromocytoma cells, nuclear staining for Trk-A was not present in conditions of serum deprivation, but could be induced by exposure to NGF or to a mixture of soluble mediators. We conclude that nuclear localization of the intracellular domain of Trk-A is observed constitutively in liver cells such as HSC, while in other cell types it could be induced in response to soluble factors.     

Identification and characterization of a novel salt‐tolerant esterase from a Tibetan glacier metagenomic library

A salt‐tolerant esterase, designated H9Est, was identified from a metagenomic library of the Karuola glacier. H9Est gene comprised 1071 bp and encoded a polypeptide of 357 amino acids with a molecular mass of 40 kDa. Sequence analysis revealed that H9Est belonged to the family IV of bacterial lypolitic enzyme. H9Est was overexpressed in Escherichia coli and the purified enzyme showed hydrolytic activity towards p‐nitrophenyl esters with carbon chain from 2 to 8. The optimal esterase activity was at 40°C and pH 8.0 and the enzyme retained its activity towards some miscible organic solvents such as polyethylene glycol. A three‐dimensional model of H9Est revealed that S200, D294, and H324 formed the H9Est catalytic triad. Circular Dichroism spectra and molecular dynamic simulation indicated that the esterase had a wide denaturation temperature range and flexible loops that would be beneficial for H9Est performance at low temperatures while retaining heat‐resistant features. © 2015 American Institute of Chemical Engineers Biotechnol. Prog., 31:890–899, 2015     

Diverging effects of human recombinant anti-hepatitis C virus (HCV) antibody fragments derived from a single patient on the infectivity of a vesicular stomatitis virus/HCV pseudotype

Hepatitis C virus (HCV) is the major causative agent of blood-borne non-A, non-B hepatitis. Although a strong humoral response is detectable within a few weeks of primary infection and during viral persistence, the role played by antibodies against HCV envelope glycoproteins in controlling viral replication is still unclear. We describe how human monoclonal anti-HCV E2 antibody fragments isolated from a chronically HCV-infected patient differ sharply in their abilities to neutralize infection of HepG2 cells by a vesicular stomatitis virus pseudotype bearing HCV envelope glycoproteins. Two clones were able to neutralize the pseudotype virus at a concentration of 10 micro g/ml, while three other clones completely lacked this activity. These data can explain the lack of protection and the possibility of reinfection that occur even in the presence of a strong antiviral antibody response.