Strains nodulating Lupinus albus on different continents belong to several new chromosomal and symbiotic lineages within Bradyrhizobium

In this work we analysed different chromosomal and symbiotic markers in rhizobial strains nodulating Lupinus albus (white lupin) in several continents. Collectively the analysis of their rrs and atpD genes, and 16S-23S intergenic spacers (ITS), showed that they belong to at least four chromosomal lineages within the genus Bradyrhizobium. Most isolates from the Canary Islands (near to the African continent) grouped with some strains isolated on mainland Spain and were identified as Bradyrhizobium canariense. These strains are divided into two ITS subgroups coincident with those previously described from isolates nodulating Ornithopus. The remaining strains isolated on mainland Spain grouped with most isolates from Chile (American continent) forming a new lineage related to Bradyrhizobium japonicum. The strains BLUT2 and ISLU207 isolated from the Canary Islands and Chile, respectively, formed two new lineages phylogenetically close to different species of Bradyrhizobium depending on the marker analyzed. The analysis of the nodC gene showed that all strains nodulating L. albus belong to the biovar genistearum; nevertheless they form four different nodC lineages of which lineage C is at present exclusively formed by L. albus endosymbionts isolated from different continents.     

Mixed human intra- and inter-subtype infections with the parasite Blastocystis sp

Because of their limitations, current subtyping methods likely underestimate mixed human intra- and inter-subtype infections with Blastocystis sp. leading to erroneous data in the context of epidemiological studies. We confirmed this hypothesis by the identification of several isolates belonging to three subtypes in a patient considered at high risk of mixed infection through her lifestyle in rural area and long history of travelling.     

Understanding type 1 diabetes through proteomics

Introduction: Auto-immunity against pancreatic beta-cells leads to an absolute shortage of the hormone insulin, resulting in hyperglycemia and the onset of type 1 diabetes (T1D). Proteomic approaches have been used to elucidate the mechanisms of beta-cell dysfunction and death.

Areas covered: In the present review, we discuss discoveries in the beta-cell proteome that have contributed to better insights in the role of the beta-cell in T1D. Techniques, such as 2D-DIGE and MALDI imaging, together with new approaches for sample preparation, including laser capture microdissection and immunopeptidomics, have resulted in novel mechanistic insights in the pathogenesis of T1D. We describe how proteomic studies in beta-cell lines as well as isolated islets from animal models and humans have discovered intracellular signaling pathways leading to beta-cell destruction, the generation of neo-antigens through post-translational modifications of beta-cell antigens as well as better biomarkers of disease progression.

Expert commentary: Proteomics has contributed to the discovery of beta-cell neo-autoantigen generation through post-translational modifications, hybrid insulin peptide formation and the generation of defective ribosomal gene products. These concepts are revolutionizing our insights in the pathogenesis of T1D, acknowledging a central role for the beta-cell in its own destruction.     

FVB.129P2-Pde6b(+) Tyr(c-ch)/Ant, a sighted variant of the FVB/N mouse strain suitable for behavioral analysis

Mice of the FVB/N strain are severely visual impaired as a result of tyrosinase gene defects, leading to a deficiency of the key enzyme for melanin synthesis in skin and eye and of cyclic guanosine monophosphate phosphodiesterase gene defects, which results in albinism (Tyr(c/c)) and retinal degeneration (Pde6b(rd1/rd1)), respectively. Nevertheless, FVB/N mice are commonly used for the generation of transgenic animals because of their large, strong pronuclei and high breeding performance. However, due to visual impairment of the FVB/N animals, the resulting transgenic animals cannot be used in tests that depend on vision, including tests of cognitive behavior. Therefore, we have bred a sighted version of the FVB/N strain by an outcross between FVB/N and 129P2/OlaHsd, followed by repeated backcrosses to FVB/N mice while selecting against albinism and homozygosity of the retinal degeneration mutation. After 11 generations of backcrossing, sighted animals were intercrossed to generate the congenic FVB.129P2-Pde6b(+) Tyr(c-ch)/Ant strain, which is pigmented (Tyr(c-ch)/(c-ch)) and devoid of the genetic predisposition to retinal degeneration. The accurate visual abilities of the FVB.129P2-Pde6b(+) Tyr(c-ch)/Ant mice, for which we propose the name FVBS/Ant, demonstrated a clear visual evoked potential in the presence of normal eye histology and improved performance in the Morris water maze test.     

Surgery and angiogenesis

Surgery may be regarded as an angiogenesis-inducing condition since it evokes the release of many angiogenic factors. Regarding the mechanistic overlap between tumor-associated neovascularisation and (physiological) angiogenesis in response to injury and hypoxia, surgery may promote the uncontrolled growth of residual dormant tumor cells. With the advent of anti-angiogenic agents, surgeons will be faced with more patients undergoing surgery for primary and secondary tumors under anti-angiogenic treatment. This could present problems with regard to angiogenesis-dependent phenomena such as wound repair, healing of intestinal anastomoses and liver regeneration. In this review we will discuss these matters from a biomedical and clinical point of view.     

A meta‐analysis of species–abundance distributions

The species–abundance distribution (SAD) describes the abundances of all species within a community. Many different models have been proposed to describe observed SADs. Best known are the logseries, the lognormal, and a variety of niche division models. They are most often visualized using either species richness – log abundance class (Preston) plots or abundance – species rank order (Whittaker) plots. Because many of the models predict very similar shapes, model distinction and testing become problematic. However, the variety of models can be classified into three basic types: one that predicts a double S‐shape in Whittaker plots and a unimodal distribution in Preston plots (the lognormal type), a second that lacks the mode in Preston plots (the logseries type), and a third that predicts power functions in both plotting types (the power law type). Despite the interest of ecologists in SADs no formal meta‐analysis of models and plotting types has been undertaken so far. Here we use a compilation of 558 species–abundance distributions from 306 published papers to infer the frequency of the three SAD shapes in dependence of environmental variables and type of plotting. Our results highlight the importance of distinguishing between fully censused and incompletely sampled communities in the study of SADs. We show that completely censused terrestrial or freshwater animal communities tend to follow lognormal type SADs more often than logseries or power law types irrespective of species richness, spatial scale, and geographic position. However, marine communities tend to follow the logseries type, while plant communities tend to follow the power law. In incomplete sets the power law fitted best in Whittaker plots, and the logseries in Preston plots. Finally our study favors the use of Whittaker over Preston plots.     

Long-term exposure to elevated zinc concentrations induced structural changes and zinc tolerance of the nitrifying community in soil

A series of long-term Zn-contaminated soils was sampled around a galvanized pylon. The potential nitrification rate (PNR) was unaffected by the soil total Zn concentrations up to 25 mmol Zn kg(-1) whereas spiking the uncontaminated control soil with ZnCl(2) to identical total concentrations completely eliminated nitrification. The larger sensitivity of the PNR to spiked ZnCl(2) than to the Zn added in the field was equally found when relating the PNR to the Zn concentrations in the pore water of these soils, suggesting differences in Zn tolerance of the nitrifying communities. Zinc tolerance in the long-term Zn-contaminated soil was demonstrated by showing that (i) the nitrifying community of long-term Zn-contaminated soil samples was less sensitive to Zn than that of the uncontaminated control soil when both communities were inoculated in sterile ZnCl(2)-contaminated soil samples, and, that (ii) addition of ZnCl(2) to the long-term Zn-contaminated soil samples affected nitrification less than equal additions of ZnCl(2) to uncontaminated control samples. Denaturing gradient gel electrophoresis fingerprinting of polymerase chain reaction amplified 16SrRNA gene fragments of ammonia-oxidizing bacteria showed that the community structure in uncontaminated and long-term contaminated soil samples was different and could be related to soil Zn concentrations.     

An Aberrant Cerebellar Development in Mice Lacking Matrix Metalloproteinase-3

Cell–cell and cell–matrix interactions are necessary for neuronal patterning and brain wiring during development. Matrix metalloproteinases (MMPs) are proteolytic enzymes capable of remodelling the pericellular environment and regulating signaling pathways through cleavage of a large degradome. MMPs have been suggested to affect cerebellar development, but the specific role of different MMPs in cerebellar morphogenesis remains unclear. Here, we report a role for MMP-3 in the histogenesis of the mouse cerebellar cortex. MMP-3 expression peaks during the second week of postnatal cerebellar development and is most prominently observed in Purkinje cells (PCs). In MMP-3 deficient (MMP-3^−/−) mice, a protracted granule cell (GC) tangential migration and a delayed GC radial migration results in a thicker and persistent external granular layer, a retarded arrival of GCs in the inner granular layer, and a delayed GABAergic interneuron migration. Importantly, these neuronal migration anomalies, as well as the consequent disturbed synaptogenesis on PCs, seem to be caused by an abnormal PC dendritogenesis, which results in reduced PC dendritic trees in the adult cerebellum. Of note, these developmental and adult cerebellar defects might contribute to the aberrant motor phenotype observed in MMP-3^−/− mice and suggest an involvement of MMP-3 in mouse cerebellar development.     

The death receptor CD95 activates the cofilin pathway to stimulate tumour cell invasion

The death receptor CD95 promotes apoptosis through well-defined signalling pathways. In colorectal cancer cells, CD95 primarily stimulates migration and invasion through pathways that are incompletely understood. Here, we identify a new CD95-activated tyrosine kinase pathway that is essential for CD95-stimulated tumour cell invasion. We show that CD95 promotes Tyr 783 phosphorylation of phospholipase C-γ1 through the platelet-derived growth factor receptor-β, resulting in ligand-stimulated phosphatidylinositol (4,5)-bisphosphate (PIP(2)) hydrolysis. PIP(2) hydrolysis liberates the actin-severing protein cofilin from the plasma membrane to initiate cortical actin remodelling. Cofilin activation is required for CD95-stimulated formation of membrane protrusions and increased tumour cell invasion.