A new phenotype of <Emphasis Type="Italic">Polymyxa betae</Emphasis> in <Emphasis Type="Italic">Arabidopsis thaliana</Emphasis>

The understanding of the molecular biology of Polymyxa betae, the protist vector of Beet necrotic yellow vein virus, remains limited because of the obligate nature of this root endoparasite and the limited data on the genome of Beta vulgaris, its most common host plant. The aim of this work was to assess the infection of P. betae in Arabidopsis thaliana in order to learn more about the P. betae genome and its interaction with the host. The susceptibility of a set of ecotypes of various origins to a monosporosorus and aviruliferous isolate of P. betae was analyzed in a series of bioassays conducted under controlled conditions. P. betae was detected in roots of A. thaliana using light microscopy and PCR. The infection severity was relatively low in this species compared with B. vulgaris, but the different stages of the life cycle were present. The phenotype of P. betae in A. thaliana root cells differed from the phenotype in B. vulgaris: the spore-forming phase was more prevalent in comparison with the sporangial phase, and the sporosori contained a lower number of spores. The compatible interaction between P. betae and A. thaliana obtained after the inoculation of zoospores and optimal conditions for the development of P. betae provide a new model system that can be used to improve the knowledge on the P. betae genome and on the mechanisms of the spore-forming phase of P. betae.     

Selective inhibition of a regulatory subunit of protein phosphatase 1 restores proteostasis

Many biological processes are regulated through the selective dephosphorylation of proteins. Protein serine-threonine phosphatases are assembled from catalytic subunits bound to diverse regulatory subunits that provide substrate specificity and subcellular localization. We describe a small molecule, guanabenz, that bound to a regulatory subunit of protein phosphatase 1, PPP1R15A/GADD34, selectively disrupting the stress-induced dephosphorylation of the α subunit of translation initiation factor 2 (eIF2α). Without affecting the related PPP1R15B-phosphatase complex and constitutive protein synthesis, guanabenz prolonged eIF2α phosphorylation in human stressed cells, adjusting the protein production rates to levels manageable by available chaperones. This favored protein folding and thereby rescued cells from protein misfolding stress. Thus, regulatory subunits of phosphatases are drug targets, a property used here to restore proteostasis in stressed cells.     

Glycolipids as receptors for Bacillus thuringiensis crystal toxin

The development of pest resistance threatens the effectiveness of Bacillus thuringiensis (Bt) toxins used in transgenic and organic farming. Here, we demonstrate that (i) the major mechanism for Bt toxin resistance in Caenorhabditis elegans entails a loss of glycolipid carbohydrates; (ii) Bt toxin directly and specifically binds glycolipids; and (iii) this binding is carbohydrate-dependent and relevant for toxin action in vivo. These carbohydrates contain the arthroseries core conserved in insects and nematodes but lacking in vertebrates. We present evidence that insect glycolipids are also receptors for Bt toxin.     

Characterization of a common susceptibility locus for asthma-related traits

Susceptibility to asthma depends on variation at an unknown number of genetic loci. To identify susceptibility genes on chromosome 7p, we adopted a hierarchical genotyping design, leading to the identification of a 133-kilobase risk-conferring segment containing two genes. One of these coded for an orphan G protein-coupled receptor named GPRA (G protein-coupled receptor for asthma susceptibility), which showed distinct distribution of protein isoforms between bronchial biopsies from healthy and asthmatic individuals. In three cohorts from Finland and Canada, single nucleotide polymorphism-tagged haplotypes associated with high serum immunoglobulin E or asthma. The murine ortholog of GPRA was up-regulated in a mouse model of ovalbumin-induced inflammation. Together, these data implicate GPRA in the pathogenesis of atopy and asthma.     

Use of genetic profiling in leprosy to discriminate clinical forms of the disease

Leprosy presents as a clinical and immunological spectrum of disease. With the use of gene expression profiling, we observed that a distinction in gene expression correlates with and accurately classifies the clinical form of the disease. Genes belonging to the leukocyte immunoglobulin-like receptor (LIR) family were significantly up-regulated in lesions of lepromatous patients suffering from the disseminated form of the infection. In functional studies, LIR-7 suppressed innate host defense mechanisms by shifting monocyte production from interleukin-12 toward interleukin-10 and by blocking antimicrobial activity triggered by Toll-like receptors. Gene expression profiles may be useful in defining clinical forms of disease and providing insights into the regulation of immune responses to pathogens.     

Host-parasite coevolutionary conflict between Arabidopsis and downy mildew

Plants are constantly exposed to attack by an array of diverse pathogens but lack a somatically adaptive immune system. In spite of this, natural plant populations do not often suffer destructive disease epidemics. Elucidating how allelic diversity within plant genes that function to detect pathogens (resistance genes) counteracts changing structures of pathogen genes required for host invasion (pathogenicity effectors) is critical to our understanding of the dynamics of natural plant populations. The RPP13 resistance gene is the most polymorphic gene analyzed to date in the model plant Arabidopsis thaliana. Here we report the cloning of the avirulence gene, ATR13, that triggers RPP13-mediated resistance, and we show that it too exhibits extreme levels of amino acid polymorphism. Evidence of diversifying selection visible in both components suggests that the host and pathogen may be locked in a coevolutionary conflict at these loci, where attempts to evade host resistance by the pathogen are matched by the development of new detection capabilities by the host.     

Influence of the Atlantic subpolar gyre on the thermohaline circulation

During the past decade, record-high salinities have been observed in the Atlantic Inflow to the Nordic Seas and the Arctic Ocean, which feeds the North Atlantic thermohaline circulation (THC). This may counteract the observed long-term increase in freshwater supply to the area and tend to stabilize the North Atlantic THC. Here we show that the salinity of the Atlantic Inflow is tightly linked to the dynamics of the North Atlantic subpolar gyre circulation. Therefore, when assessing the future of the North Atlantic THC, it is essential that the dynamics of the subpolar gyre and its influence on the salinity are taken into account.