Body size determines the strength of the latitudinal diversity gradient

In most groups of organisms, the species richness decreases from the tropics to the poles. The mechanisms causing this latitudinal diversity gradient are still controversial. We present data from a comprehensive weighted meta-analysis on the strength of the latitudinal gradient in relation to body size. We sampled literature data on the correlation between species richness and latitude for a variety of organisms, ranging from trees to protozoa. In addition, own data on the presence of large-scale diversity patterns for diatoms were included, both for local and regional species richness. The strength of the latitudinal gradient was positively correlated to the size of the organisms. Strongest decreases of species richness to the poles was found for large organisms like trees and vertebrates, whereas meiofauna, protozoa and diatoms showed weak or no correlations between species richness and latitude. These results imply that latitudinal gradients are shaped by non-equilibrium (regional) processes and are persistent under conditions of dispersal limitation.     

Navigating the complexity of ecological stability

Human actions challenge nature in many ways. Ecological responses are ineluctably complex, demanding measures that describe them succinctly. Collectively, these measures encapsulate the overall ‘stability’ of the system. Many international bodies, including the Intergovernmental Science‐Policy Platform on Biodiversity and Ecosystem Services, broadly aspire to maintain or enhance ecological stability. Such bodies frequently use terms pertaining to stability that lack clear definition. Consequently, we cannot measure them and so they disconnect from a large body of theoretical and empirical understanding. We assess the scientific and policy literature and show that this disconnect is one consequence of an inconsistent and one‐dimensional approach that ecologists have taken to both disturbances and stability. This has led to confused communication of the nature of stability and the level of our insight into it. Disturbances and stability are multidimensional. Our understanding of them is not. We have a remarkably poor understanding of the impacts on stability of the characteristics that define many, perhaps all, of the most important elements of global change. We provide recommendations for theoreticians, empiricists and policymakers on how to better integrate the multidimensional nature of ecological stability into their research, policies and actions.     

Loss of all three APP family members during development impairs synaptic function and plasticity,disrupts learning,and causes an autism‐like phenotype

The key role of APP for Alzheimer pathogenesis is well established. However, perinatal lethality of germline knockout mice lacking the entire APP family has so far precluded the analysis of its physiological functions for the developing and adult brain. Here, we generated conditional APP/APLP1/APLP2 triple KO (cTKO) mice lacking the APP family in excitatory forebrain neurons from embryonic day 11.5 onwards. NexCre cTKO mice showed altered brain morphology with agenesis of the corpus callosum and disrupted hippocampal lamination. Further, NexCre cTKOs revealed reduced basal synaptic transmission and drastically reduced long‐term potentiation that was associated with reduced dendritic length and reduced spine density of pyramidal cells. With regard to behavior, lack of the APP family leads not only to severe impairments in a panel of tests for learning and memory, but also to an autism‐like phenotype including repetitive rearing and climbing, impaired social communication, and deficits in social interaction. Together, our study identifies essential functions of the APP family during development, for normal hippocampal function and circuits important for learning and social behavior.     

Identification of phospholipase C gamma1 as a protein tyrosine phosphatase mu substrate that regulates cell migration

The receptor protein tyrosine phosphatase PTPµ has a cell‐adhesion molecule‐like extracellular segment and a catalytically active intracellular segment. This structure gives PTPµ the ability to transduce signals in response to cell–cell adhesion. Full‐length PTPµ is down‐regulated in glioma cells by proteolysis which is linked to increased migration of these cells in the brain. To gain insight into the substrates PTPµ may be dephosphorylating to suppress glioma cell migration, we used a substrate trapping method to identify PTPµ substrates in tumor cell lines. We identified both PKCδ and PLCγ1 as PTPµ substrates. As PLCγ1 activation is linked to increased invasion of cancer cells, we set out to determine whether PTPµ may be upstream of PLCγ1 in regulating glioma cell migration. We conducted brain slice assays using U87‐MG human glioma cells in which PTPµ expression was reduced by shRNA to induce migration. Treatment of the same cells with PTPµ shRNA and a PLCγ1 inhibitor prevented migration of the cells within the brain slice. These data suggest that PLCγ1 is downstream of PTPµ and that dephosphorylation of PLCγ1 is likely to be a major pathway through which PTPµ suppresses glioma cell migration. J. Cell. Biochem. 112: 39–48, 2011. © 2010 Wiley‐Liss, Inc.     

DNA staining in agarose gels with Zn²+-cyclen-pyrene

A pyrene-labeled Zn2+-cyclen complex for the staining of DNA in agarose gels is reported. The metal chelate coordinates reversibly to the DNA phosphate backbone, which induces the formation of pyrene excimers. The typical pyrene excimer emission is used for the detection of the DNA. Staining is limited to agarose gels and is less sensitive than ethidium bromide, but DNA amounts as low as 10 ng and short DNA strands (～300 b.p.) are detectable. Gel extraction as a standard technique in molecular biology was successfully performed after staining with Zn2+-cyclen-pyrene. Cytotoxicity tests on HeLa and V-79 cells reveal that the zinc-cyclen pyrene probe is significant less toxic compared to ethidium bromide.     

Altered complementary feeding strategies of the consumers <Emphasis Type="Italic">Hydrobia ulvae</Emphasis> and <Emphasis Type="Italic">Idotea emarginata</Emphasis> via passive selectivity

This study aimed to identify differences in selectivity, foraging behaviour and complementary feeding of two benthic consumers (the isopod Idotea emarginata and the snail Hydrobia ulvae) using traditional cell counting as an indicator for algal biomass reduction and stable isotope labelling to detect differences in assimilation and digestion. We hypothesized that even when active feeding preferences of food components are not apparent, passive selectivity via mechanisms such as food assimilation and digestion can be of relevance. Algal biomass was reduced to a similar degree by the grazers independently from grazer and prey combinations without any indication for an active choice of food components. However, the isotope labelling approach indicated that passive selectivity can alter complementary feeding strategies, as we detected shifts in feeding preferences in relation to food quantity and competition. Thus, stable isotope labelling of food components opens up new perspectives in community ecology, allowing assessment of such complex mechanisms as passive selectivity, complementary feeding and competition.     

Sulfatide Recognition by Colonization Factor Antigen CS6 from Enterotoxigenic Escherichia coli

The first step in the pathogenesis of enterotoxigenic Escherichia coli (ETEC) infections is adhesion of the bacterium to the small intestinal epithelium. Adhesion of ETEC is mediated by a number of antigenically distinct colonization factors, and among these, one of the most commonly detected is the non-fimbrial adhesin coli surface antigen 6 (CS6). The potential carbohydrate recognition by CS6 was investigated by binding of recombinant CS6-expressing E. coli and purified CS6 protein to a large number of variant glycosphingolipids separated on thin-layer chromatograms. Thereby, a highly specific binding of the CS6-expressing E. coli, and the purified CS6 protein, to sulfatide (SO₃-3Galβ1Cer) was obtained. The binding of the CS6 protein and CS6-expressing bacteria to sulfatide was inhibited by dextran sulfate, but not by dextran, heparin, galactose 4-sulfate or galactose 6-sulfate. When using recombinantly expressed and purified CssA and CssB subunits of the CS6 complex, sulfatide binding was obtained with the CssB subunit, demonstrating that the glycosphingolipid binding capacity of CS6 resides within this subunit. CS6-binding sulfatide was present in the small intestine of species susceptible to CS6-mediated infection, e.g. humans and rabbits, but lacking in species not affected by CS6 ETEC, e.g. mice. The ability of CS6-expressing ETEC to adhere to sulfatide in target small intestinal epithelium may thus contribute to virulence.