Local conditions matter: Minimal and variable effects of soil disturbance on microbial communities and functions in European vineyards.

Soil tillage or herbicide applications are commonly used in agriculture for weed control. These measures may also represent a disturbance for soil microbial communities and their functions. However, the generality of response patterns of microbial communities and functions to disturbance have rarely been studied at large geographical scales. We investigated how a soil disturbance gradient (low, intermediate, high), realized by either tillage or herbicide application, affects diversity and composition of soil bacterial and fungal communities as well as soil functions in vineyards across five European countries. Microbial alpha-diversity metrics responded to soil disturbance sporadically, but inconsistently across countries. Increasing soil disturbance changed soil microbial community composition at the European level. However, the effects of soil disturbance on the variation of microbial communities were smaller compared to the effects of location and soil covariates. Microbial respiration was consistently impaired by soil disturbance, while effects on decomposition of organic substrates were inconsistent and showed positive and negative responses depending on the respective country. Therefore, we conclude that it is difficult to extrapolate results from one locality to others because microbial communities and environmental conditions vary strongly over larger geographical scales.

Biodiversity effects on grape quality depend on variety and management intensity.

Interactions between plants can be beneficial, detrimental or neutral. In agricultural systems, competition between crop and spontaneous vegetation is a major concern. We evaluated the relative support for three non-exclusive ecological hypotheses about interactions between crop and spontaneous plants based on competition, complementarity or facilitation.The study was conducted in Swiss vineyards with different vegetation management intensities. In all, 33 vineyards planted with two different grape varieties were studied over 3 years to determine whether low-intensity vegetation management might provide benefits for grape quality parameters. Management intensity varied with the degree of control of spontaneous inter-row vegetation. Features of spontaneous vegetation measured included total cover, total species richness and abundance of nitrogen-fixing plants. Grape quality parameters of known importance to wine making (yeast assimilable nitrogen, sugars, tartaric acid and malic acid) were determined by Fourier-transform infrared spectroscopy (FTIR). Using structural equation modelling, we evaluated hypotheses about the multivariate responses of grape quality parameters as well as the direct and indirect (plant-mediated) effects of management.Observed effects of management differed between grape varieties. Management intensity and abundance of N-fixing plants significantly influenced grape quality parameters while total richness of spontaneous plants did not have detectable effects. Abundance of N-fixing plants was enhanced by low-intensity management resulting in increased N content in the red grape variety Pinot noir, potentially enhancing grape quality, while measured soil N content did not explain the increase.Synthesis and applications. Our study shows that crop quality can be enhanced by spontaneous plants, in this case by the abundance of a key functional group (N-fixers), most likely through plant-plant or plant-microbe facilitation. However, beneficial interactions may have a high specificity in terms of facilitation partners and may have contrasting effects at low taxonomic resolutions such as crop varieties. Generally, increasing plant biodiversity in agricultural systems may increase competition with crops. Thus, the identification of suitable interaction partners and a careful balance between crop variety and spontaneous plant species may be necessary to utilize beneficial interactions and to reduce the trade-off between agricultural production and biodiversity to achieve a sustainable ecological benefit in agricultural systems.

Impaired proteoglycan glycosylation, elevated TGF-ß signaling, and abnormal osteoblast differentiation as the basis for bone fragility in a mouse model for gerodermia osteodysplastica.

Gerodermia osteodysplastica (GO) is characterized by skin laxity and early-onset osteoporosis. GORAB, the responsible disease gene, encodes a small Golgi protein of poorly characterized function. To circumvent neonatal lethality of the GorabNull full knockout, Gorab was conditionally inactivated in mesenchymal progenitor cells (Prx1-cre), pre-osteoblasts (Runx2-cre), and late osteoblasts/osteocytes (Dmp1-cre), respectively. While in all three lines a reduction in trabecular bone density was evident, only GorabPrx1 and GorabRunx2 mutants showed dramatically thinned, porous cortical bone and spontaneous fractures. Collagen fibrils in the skin of GorabNull mutants and in bone of GorabPrx1 mutants were disorganized, which was also seen in a bone biopsy from a GO patient. Measurement of glycosaminoglycan contents revealed a reduction of dermatan sulfate levels in skin and cartilage from GorabNull mutants. In bone from GorabPrx1 mutants total glycosaminoglycan levels and the relative percentage of dermatan sulfate were both strongly diminished. Accordingly, the proteoglycans biglycan and decorin showed reduced glycanation. Also in cultured GORAB-deficient fibroblasts reduced decorin glycanation was evident. The Golgi compartment of these cells showed an accumulation of decorin, but reduced signals for dermatan sulfate. Moreover, we found elevated activation of TGF-ß in GorabPrx1 bone tissue leading to enhanced downstream signalling, which was reproduced in GORAB-deficient fibroblasts. Our data suggest that the loss of Gorab primarily perturbs pre-osteoblasts. GO may be regarded as a congenital disorder of glycosylation affecting proteoglycan synthesis due to delayed transport and impaired posttranslational modification in the Golgi compartment.

Mutations in WNT1 cause different forms of bone fragility.

We report that hypofunctional alleles of WNT1 cause autosomal-recessive osteogenesis imperfecta, a congenital disorder characterized by reduced bone mass and recurrent fractures. In consanguineous families, we identified five homozygous mutations in WNT1: one frameshift mutation, two missense mutations, one splice-site mutation, and one nonsense mutation. In addition, in a family affected by dominantly inherited early-onset osteoporosis, a heterozygous WNT1 missense mutation was identified in affected individuals. Initial functional analysis revealed that altered WNT1 proteins fail to activate canonical LRP5-mediated WNT-regulated ß-catenin signaling. Furthermore, osteoblasts cultured in vitro showed enhanced Wnt1 expression with advancing differentiation, indicating a role of WNT1 in osteoblast function and bone development. Our finding that homozygous and heterozygous variants in WNT1 predispose to low-bone-mass phenotypes might advance the development of more effective therapeutic strategies for congenital forms of bone fragility, as well as for common forms of age-related osteoporosis.

Cell polarity development and protein trafficking in hepatocytes lacking E-cadherin/beta-catenin-based adherens junctions.

Using a mutant hepatocyte cell line in which E-cadherin and beta-catenin are completely depleted from the cell surface, and, consequently, fail to form adherens junctions, we have investigated adherens junction requirement for apical-basolateral polarity development and polarized membrane trafficking. It is shown that these hepatocytes retain the capacity to form functional tight junctions, develop full apical-basolateral cell polarity, and assemble a subapical cortical F-actin network, although with a noted delay and a defect in subsequent apical lumen remodeling. Interestingly, whereas hepatocytes typically target the plasma membrane protein dipeptidyl peptidase IV first to the basolateral surface, followed by its transcytosis to the apical domain, hepatocytes lacking E-cadherin-based adherens junctions target dipeptidyl peptidase IV directly to the apical surface. Basolateral surface-directed transport of other proteins or lipids tested was not visibly affected in hepatocytes lacking E-cadherin-based adherens junctions. Together, our data show that E-cadherin/beta-catenin-based adherens junctions are dispensable for tight junction formation and apical lumen biogenesis but not for apical lumen remodeling. In addition, we suggest a possible requirement for E-cadherin/beta-catenin-based adherens junctions with regard to the indirect apical trafficking of specific proteins in hepatocytes.