Sex differences in learning in chimpanzees

The wild chimpanzees in Gombe National Park, Tanzania, fish for termites with flexible tools that they make out of vegetation, inserting them into the termite mound and then extracting and eating the termites that cling to the tool. Tools may be used in different ways by different chimpanzee communities according to the local chimpanzee culture. Here we describe the results of a four-year longitudinal field study in which we investigated how this cultural behaviour is learned by the community's offspring. We find that there are distinct sex-based differences, akin to those found in human children, in the way in which young chimpanzees develop their termite-fishing skills.     

The netrin receptor UNC5B mediates guidance events controlling morphogenesis of the vascular system

Blood vessels and nerves are complex, branched structures that share a high degree of anatomical similarity. Guidance of vessels and nerves has to be exquisitely regulated to ensure proper wiring of both systems. Several regulators of axon guidance have been identified and some of these are also expressed in endothelial cells; however, the extent to which their guidance functions are conserved in the vascular system is still incompletely understood. We show here that the repulsive netrin receptor UNC5B is expressed by endothelial tip cells of the vascular system. Disruption of the Unc5b gene in mice, or of Unc5b or netrin-1a in zebrafish, leads to aberrant extension of endothelial tip cell filopodia, excessive vessel branching and abnormal navigation. Netrin-1 causes endothelial filopodial retraction, but only when UNC5B is present. Thus, UNC5B functions as a repulsive netrin receptor in endothelial cells controlling morphogenesis of the vascular system.     

Influence of PPCA inhibitor on CaCO3 scale surface deposition and bulk precipitation at elevated temperature

Scale formation is a serious and costly problem encountered in the oil and gas industry. Polyphosphinocarboxylic acid (PPCA) is a common commercial organic scale inhibitor used in the oil and gas industry which is normally referred to a nucleation inhibitor. In this paper, the effect of PPCA on calcium carbonate scale is studied systematically and some new insights into the mechanisms of PPCA inhibition are given. Traditionally, the studies of scale formation and inhibition have focused on bulk precipitation or surface deposition. Few studies have focused on the difference between surface deposition and bulk precipitation processes. In this paper, the effect of PPCA inhibitor on calcium carbonate scale formation is studied both in the bulk solution and on the metal surface in supersaturated scale formation solutions which represent typical waters encountered in oil and gas production. It is clear that PPCA inhibits both bulk precipitation and surface deposition but to a different degree. At 4 ppm PPCA, the inhibition efficiency of surface deposition is greater than the inhibition efficiency of bulk precipitation. It is assumed that the inhibitor film formed on the metal surface at the highest concentration of PPCA (4 ppm) prevent the adsorption of scale crystals on the metal surface. In addition, PPCA suppresses aragonite and calcite crystal formation and results in the least stable vaterite crystal dominating the scale.     

Resource-based niches provide a basis for plant species diversity and dominance in arctic tundra.

Ecologists have long been intrigued by the ways co-occurring species divide limiting resources. Such resource partitioning, or niche differentiation, may promote species diversity by reducing competition. Although resource partitioning is an important determinant of species diversity and composition in animal communities, its importance in structuring plant communities has been difficult to resolve. This is due mainly to difficulties in studying how plants compete for below-ground resources. Here we provide evidence from a 15N-tracer field experiment showing that plant species in a nitrogen-limited, arctic tundra community were differentiated in timing, depth and chemical form of nitrogen uptake, and that species dominance was strongly correlated with uptake of the most available soil nitrogen forms. That is, the most productive species used the most abundant nitrogen forms, and less productive species used less abundant forms. To our knowledge, this is the first documentation that the composition of a plant community is related to partitioning of differentially available forms of a single limiting resource.     

Antidepressant drugs elevate rat pineal and plasma melatonin

Summary Acute administration in the mid-light phase of a number of antidepressant drugs of different pharmacological profiles elevated pineal and plasma melatonin (measured by radioimmunoassay). Following chronic treatment with the tricyclic antidepressant clomipramine, the elevation was significantly reduced. This may be an effect of reduced -adrenergic receptor sensitivity after chronic clomipramine administration, analogous to other findings of reduced -adrenergic receptor binding and reduced noradrenaline-sensitive adenylate-cyclase response.These collaborative studies were made possible by a Twinning Grant from the European Training Programme for Brain and Behaviour Research; J.A. was supported by the Medical Research Council of Great Britain. We thank M. Lichtsteiner for excellent technical assistance. This paper was written during a Fellowship of the Swiss Biomedical Research Foundation to A.W.-J. Hofmann-LaRoche AG, Basel kindly provided the 1-5HTP-ester (Ro 11-5940) and Ro 11-2465, CIBA-Geigy AG, Basel, the maprotiline, clomipramine, and imipramine, USV, New York, the desmethylimipramine.     

Angiogenesis selectively requires the p110alpha isoform of PI3K to control endothelial cell migration

Phosphoinositide 3-kinases (PI3Ks) signal downstream of multiple cell-surface receptor types. Class IA PI3K isoforms couple to tyrosine kinases and consist of a p110 catalytic subunit (p110alpha, p110beta or p110delta), constitutively bound to one of five distinct p85 regulatory subunits. PI3Ks have been implicated in angiogenesis, but little is known about potential selectivity among the PI3K isoforms and their mechanism of action in endothelial cells during angiogenesis in vivo. Here we show that only p110alpha activity is essential for vascular development. Ubiquitous or endothelial cell-specific inactivation of p110alpha led to embryonic lethality at mid-gestation because of severe defects in angiogenic sprouting and vascular remodelling. p110alpha exerts this critical endothelial cell-autonomous function by regulating endothelial cell migration through the small GTPase RhoA. p110alpha activity is particularly high in endothelial cells and preferentially induced by tyrosine kinase ligands (such as vascular endothelial growth factor (VEGF)-A). In contrast, p110beta in endothelial cells signals downstream of G-protein-coupled receptor (GPCR) ligands such as SDF-1alpha, whereas p110delta is expressed at low level and contributes only minimally to PI3K activity in endothelial cells. These results provide the first in vivo evidence for p110-isoform selectivity in endothelial PI3K signalling during angiogenesis.     

Celiac disease patient IgA antibodies induce endothelial adhesion and cell polarization defects via extracellular transglutaminase 2

We have recently found that celiac disease patient serum-derived autoantibodies targeted against transglutaminase 2 interfere with several steps of angiogenesis, including endothelial sprouting and migration, though the mechanism involved remained to be fully characterized. This study now investigated the processes underlying the antiangiogenic effects exerted by celiac disease patient antibodies on endothelial cells, with particular regard to the adhesion, migration, and polarization signaling pathway. We observed that celiac IgA reduced endothelial cell numbers by affecting adhesion without increasing apoptosis. Endothelial cells in the presence of celiac IgA showed weak attachment, a high susceptibility to detach from fibronectin, and a disorganized extracellular matrix due to a reduction of protein cross-links. Furthermore, celiac patient IgA led to secretion of active transglutaminase 2 from endothelial cells into the culture supernatants. Additionally, cell surface transglutaminase 2 mediated integrin clustering in the presence of celiac IgA was coupled to augmented expression of β1-integrin. We also observed that celiac patient IgA-treated endothelial cells had migratory defects and a less polarized phenotype when compared to control groups, and this was associated with the RhoA signaling pathway. These biological effects mediated by celiac IgA on endothelial cells were partially influenced but not completely abolished by R281, an irreversible extracellular transglutaminase 2 enzymatic activity inhibitor. Taken together, our results imply that celiac patient IgA antibodies disturb the extracellular protein cross-linking function of transglutaminase 2, thus altering cell-extracellular matrix interactions and thereby affecting endothelial cell adhesion, polarization, and motility.     

Tetraspanin TSPAN12 regulates tumor growth and metastasis and inhibits β-catenin degradation

Ablation of tetraspanin protein TSPAN12 from human MDA-MB-231 cells significantly decreased primary tumor xenograft growth, while increasing tumor apoptosis. Furthermore, TSPAN12 removal markedly enhanced tumor-endothelial interactions and increased metastasis to mouse lungs. TSPAN12 removal from human MDA-MB-231 cells also caused diminished association between FZD4 (a key canonical Wnt pathway receptor) and its co-receptor LRP5. The result likely explains substantially enhanced proteosomal degradation of β-catenin, a key effecter of canonical Wnt signaling. Consistent with disrupted canonical Wnt signaling, TSPAN12 ablation altered expression of LRP5, Naked 1 and 2, DVL2, DVL3, Axin 1, and GSKβ3 proteins. TSPAN12 ablation also altered expression of several genes regulated by β-catenin (e.g. CCNA1, CCNE2, WISP1, ID4, SFN, ME1) that may help to explain altered tumor growth and metastasis. In conclusion, these results provide the first evidence for TSPAN12 playing a role in supporting primary tumor growth and suppressing metastasis. TSPAN12 appears to function by stabilizing FZD4–LRP5 association, in support of canonical Wnt-pathway signaling, leading to enhanced β-catenin expression and function.     

Endothelial signaling and the molecular basis of arteriovenous malformation

Arteriovenous malformations occur when abnormalities of vascular patterning result in the flow of blood from arteries to veins without an intervening capillary bed. Recent work has revealed the importance of the Notch and TGF-β signaling pathways in vascular patterning. Specifically, Notch signaling has an increasingly apparent role in arterial specification and suppression of branching, whereas TGF-β is implicated in vascular smooth muscle development and remodeling under angiogenic stimuli. These physiologic roles, consequently, have implicated both pathways in the pathogenesis of arteriovenous malformation. In this review, we summarize the studies of endothelial signaling that contribute to arteriovenous malformation and the roles of genes implicated in their pathogenesis. We further discuss how endothelial signaling may contribute to vascular smooth muscle development and how knowledge of signaling pathways may provide us targets for medical therapy in these vascular lesions.