How Stomaphis aphids use their giant proboscides

To penetrate tree bark, arboreal aphids of the genus Stomaphis Walk. (Hemiptera: Aphididae: Lachninae) have proboscides up to three times their body length. Our observations of S. quercus (L.) complement a recent analysis of the anatomy and function of these mouthparts by clarifying how these relatively short-legged aphids move their proboscides between the resting position, pointing back, and the prognathous working position. The absence of crumenae in Stomaphis aphids and their feeding technique are discussed.     

Vesicular restriction of synaptobrevin suggests a role for calcium in membrane fusion

Release of neurotransmitter occurs when synaptic vesicles fuse with the plasma membrane. This neuronal exocytosis is triggered by calcium and requires three SNARE (soluble-N-ethylmaleimide-sensitive factor attachment protein receptors) proteins: synaptobrevin (also known as VAMP) on the synaptic vesicle, and syntaxin and SNAP-25 on the plasma membrane. Neuronal SNARE proteins form a parallel four-helix bundle that is thought to drive the fusion of opposing membranes. As formation of this SNARE complex in solution does not require calcium, it is not clear what function calcium has in triggering SNARE-mediated membrane fusion. We now demonstrate that whereas syntaxin and SNAP-25 in target membranes are freely available for SNARE complex formation, availability of synaptobrevin on synaptic vesicles is very limited. Calcium at micromolar concentrations triggers SNARE complex formation and fusion between synaptic vesicles and reconstituted target membranes. Although calcium does promote interaction of SNARE proteins between opposing membranes, it does not act by releasing synaptobrevin from synaptic vesicle restriction. Rather, our data suggest a mechanism in which calcium-triggered membrane apposition enables syntaxin and SNAP-25 to engage synaptobrevin, leading to membrane fusion.     

The coming acceleration of global population ageing

The future paths of population ageing result from specific combinations of declining fertility and increasing life expectancies in different parts of the world. Here we measure the speed of population ageing by using conventional measures and new ones that take changes in longevity into account for the world as a whole and for 13 major regions. We report on future levels of indicators of ageing and the speed at which they change. We show how these depend on whether changes in life expectancy are taken into account. We also show that the speed of ageing is likely to increase over the coming decades and to decelerate in most regions by mid-century. All our measures indicate a continuous ageing of the world's population throughout the century. The median age of the world's population increases from 26.6 years in 2000 to 37.3 years in 2050 and then to 45.6 years in 2100, when it is not adjusted for longevity increase. When increases in life expectancy are taken into account, the adjusted median age rises from 26.6 in 2000 to 31.1 in 2050 and only to 32.9 in 2100, slightly less than what it was in the China region in 2005. There are large differences in the regional patterns of ageing. In North America, the median age adjusted for life expectancy change falls throughout almost the entire century, whereas the conventional median age increases significantly. Our assessment of trends in ageing is based on new probabilistic population forecasts. The probability that growth in the world's population will end during this century is 88%, somewhat higher than previously assessed. After mid-century, lower rates of population growth are likely to coincide with slower rates of ageing.     

Inverse computation and the Universal Resolving Algorithm

We survey fundamental concepts for inverse programming and then present the Universal Resolving Algorithm, an algorithm for inverse computation in a first-order, functional programming language. We discuss the key concepts of the algorithm, including a three-step approach based on the notion of a perfect process tree, and demonstrate our implementation with several examples of inverse computation.     

Adsorption-induced scission of carbon-carbon bonds

Covalent carbon-carbon bonds are hard to break. Their strength is evident in the hardness of diamonds and tensile strength of polymeric fibres; on the single-molecule level, it manifests itself in the need for forces of several nanonewtons to extend and mechanically rupture one bond. Such forces have been generated using extensional flow, ultrasonic irradiation, receding meniscus and by directly stretching a single molecule with nanoprobes. Here we show that simple adsorption of brush-like macromolecules with long side chains on a substrate can induce not only conformational deformations, but also spontaneous rupture of covalent bonds in the macromolecular backbone. We attribute this behaviour to the fact that the attractive interaction between the side chains and the substrate is maximized by the spreading of the side chains, which in turn induces tension along the polymer backbone. Provided the side-chain densities and substrate interaction are sufficiently high, the tension generated will be strong enough to rupture covalent carbon-carbon bonds. We expect similar adsorption-induced backbone scission to occur for all macromolecules with highly branched architectures, such as brushes and dendrimers. This behaviour needs to be considered when designing surface-targeted macromolecules of this type-either to avoid undesired degradation, or to ensure rupture at predetermined macromolecular sites.     

Recruitment and regulation of phosphatidylinositol phosphate kinase type 1 gamma by the FERM domain of talin

Membrane phosphoinositides control a variety of cellular processes through the recruitment and/or regulation of cytosolic proteins. One mechanism ensuring spatial specificity in phosphoinositide signalling is the targeting of enzymes that mediate their metabolism to specific subcellular sites. Phosphatidylinositol phosphate kinase type 1 gamma (PtdInsPKI gamma) is a phosphatidylinositol-4-phosphate 5-kinase that is expressed at high levels in brain, and is concentrated at synapses. Here we show that the predominant brain splice variant of PtdInsPKI gamma (PtdInsPKI gamma-90) binds, by means of a short carboxy-terminal peptide, to the FERM domain of talin, and is strongly activated by this interaction. Talin, a principal component of focal adhesion plaques, is also present at synapses. PtdInsPKI gamma-90 is expressed in non-neuronal cells, albeit at much lower levels than in neurons, and is concentrated at focal adhesion plaques, where phosphatidylinositol-4,5-bisphosphate has an important regulatory role. Overexpression of PtdInsPKI gamma-90, or expression of its C-terminal domain, disrupts focal adhesion plaques, probably by local disruption of normal phosphoinositide balance. These findings define an interaction that has a regulatory role in cell adhesion and suggest new similarities between molecular interactions underlying synaptic junctions and general mechanisms of cell adhesion.