University of Maryland, College Park

A neuroscientist marvels at our ability to learn unnatural tasks.

I find driving mind-boggling. As a neuroscientist studying motor control, I am amazed that nervous systems can adapt to the unnatural demands of operating a car. After all, humans did not evolve in habitats with steering wheels or accelerator pedals. What makes our ability to drive so curious is that it requires the modification of reflexes — twisting the steering wheel, for instance, rather than jumping aside, when an obstacle approaches.

Mark Wagner and Maurice Smith have shed some light on this curiosity. They show that the brain generalizes unnatural physical regimes, such as driving, to produce an appropriate corrective response to an unexpected change, even when that change has not been met before (M. J. Wagner and M. A. Smith J. Neurosci. 28, 10663–10673; 2008).

The duo trained undergraduates to reach quickly for a target with one hand while holding on to a motorized arm with the other. The faster the students reached, the stronger the motorized arm pushed them off course.

Initially, the students made large errors, but they soon compensated for the lateral forces. Were their brains learning the dynamics of the new force, though, or were they reassigning the activation of muscles in the spinal cord from those for reaching towards those that normally help to generate sideways pushes?

Surprising the students with a sudden pulse of force in the reaching direction provided an answer. They compensated with almost ideal corrective forces, which spinal reflexes alone could not have achieved. The slight delay in the students' responses also indicates that their brains were working from an internal model of the new force regime. How the brain develops such a model is unknown, but this paper should drive that research.

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Albert Einstein College of Medicine, New York City

A biologist considers a link between jumping genes and immune-system enzymes.

Many viruses present a fierce threat to the body. They contain nucleic acids that, when free to roam in a cell's cytoplasm, elicit an immune response involving proteins called interferons. Pairings of the nucleic-acid residues cytosine and guanine are especially good at this, unless they carry a chemical modification in the form of a methyl group. This modification is the norm for 'jumping genes', or retrotransposons, which can move around the human genome and were probably once viral genes themselves.

A team led by Daniel Stetson at the University of Washington in Seattle has uncovered a useful twist to this tale. While searching for proteins that interact with cytoplasmic nucleic acids, the researchers came across Trex1. Mutated versions of Trex1 are known to cause chilblain lupus in humans, and in mice lead to autoimmune myocarditis, whereby the immune system attacks the heart. Stetson et al. say that mice lacking Trex1 have huge numbers of retrotransposons in their heart muscles.

Critically, the authors' molecular surveys reveal that Trex1 suppresses the rate at which jumping genes move around. This indicates that Trex1 protects the body from misidentifying its own parts as 'foreign' by degrading retrotransposons and thus preventing them from overloading the system (D. B. Stetson et al. Cell 134, 587–598; 2008).

That jumping genes have the potential to overwhelm the system in this way was unexpected. Most experts had assumed that the addition of methyl groups took care of quenching them. But if retrotransposons are made at a rate that triggers inflammation, as Stetson and his colleagues' experiments propose, it could open up a whole new avenue for research. Everyone studying lupus and related diseases should be excited.

Posted by Anna Petherick at 05:11 PM | Permalink | Comments (0) | TrackBacks (0)

Washington University, St Louis, Missouri

A planetary scientist has big hopes for a little world.

Right now, the most exciting object in the Solar System is Saturn's diminutive moon Enceladus. Its deformed south polar region emits copious amounts of heat along the length of several young, active ridges and fractures, as well as plumes of tiny ice particles, water vapour and other chemicals.

The Cassini spacecraft — equipped with plume-gas and particle analysers and clever imaging gadgetry — is currently in the neighbourhood. Seizing this opportunity, Gabriel Tobie of the University of Nantes in France and his colleagues have incorporated some of its recent measurements into theoretical models of tidal heat production on Enceladus (G. Tobie et al. Icarus 196, 642–652; 2008). Only the ebb and flow of tides could properly account for such prodigious geological activity on an icy moon that measures just 500 kilometres in diameter.

The authors start with the generally accepted idea that Enceladus has differentiated into a rock core and an icy mantle. They then show that the size of the tidal motion of the mantle is inadequate to generate the observed thermal emission, so there must be a fluid ocean sandwiched between the two solid layers. This is no great surprise, but Tobie et al. go further, showing that even if the mantle is made soft and deformable over the southern polar region (as the ice would be if it were relatively warm), a sandwiched, liquid ocean must reach at least as far as around the entire southern hemisphere.

The team imagines that, below Enceladus's south pole, tidal heating concentrates in warm, upwelling, convectively mobile ice. This, in turn, causes the cold, brittle surface layer to rupture — and the exposed warm ice sublimates, releasing trapped gases. It is a compelling picture, and one that promises to help unlock the internal activity of other icy satellites.

Posted by Anna Petherick at 05:09 PM | Permalink | Comments (0) | TrackBacks (0)

INSERM, Paris

An immunologist applauds a protein that prunes intolerant white blood cells.

Spreading tolerance is a worthy cause. In the body, newly made white blood cells are rendered tolerant to the many thousands of native proteins. But, like any complex process, this one is not foolproof, and when it goes wrong intolerant white cells cause autoimmune disease.

One way that the tolerancespreading system can fail is by not having enough 'field agents' to pick off intolerant dissenters. Regulatory T lymphocytes (Treg), a type of white blood cell, are these field agents. They find and suppress other white cells that react to healthy parts of the body. Although it is known that people with low Treg levels tend to have autoimmune diseases, how the cells function has been unclear. Recently, however, researchers in Japan shed light on this mystery.

Kajsa Wing, now at the Karolinska Institute in Stockholm, and her colleagues focused on the protein CTLA-4, which is preferentially expressed by Treg cells and forms part of a rheumatoid arthritis drug called Abatacept. They bred mice without CTLA-4 on the surface of their Treg cells. The animals appeared healthy until maturity, then quickly developed autoimmunity. So CTLA-4 is needed for the field-agent system to operate, and merely expressing it in smaller quantities on other sorts of white blood cell isn't enough. Wing et al. then discovered that CTLA-4 on Treg cells interacts with and diminishes two proteins, CD80 and CD86, on the surface of dentritic cells, which show other white cells what to hunt (K. Wing et al. Science 322, 271–275; 2008).

All of this confirms that CTLA-4 should provide a means of treating autoimmune diseases. Blocking CTLA-4 should improve the capacity of dendritic cells to present dangerous native cells to the immune system. Clinical trials for cancer treatments that do just that are already under way. Now we have a clearer idea how they work.

Posted by Anna Petherick at 05:06 PM | Permalink | Comments (0) | TrackBacks (0)

Rice University, Houston, Texas

A physicist foresees a new era in electronics.

A material's electronic properties depend largely on its density of mobile charge carriers (electrons and holes). The most common way of tuning that density is 'doping'. This involves carefully adding atoms or molecules that donate or take up electrons from the surrounding material. But doping comes with a downside: these added impurities themselves become charged, so they scatter mobile charge carriers and muddy the predictability of the material's electronic properties.

How to avoid doping? Look to Julius Edgar Lilienfield. In 1925, he proposed what is now called the 'field effect', in which the material of interest functions as one electrode of a capacitor. When a voltage is applied to the other electrode, equal and opposite charge densities accumulate on the sample material. The density of charge carriers can be varied as it is in doping, but not to the same extent. Nonetheless, the field effect has an everyday role in transistors — which are the fundamental parts of consumer electronics.

Another of Lilienfield's inventions, the electrolytic capacitor, holds the key to much higher field-effect charge densities, which could have dramatic consequences. Researchers at Tohoku University in Sendai, Japan, recently used a polymer electrolyte to achieve sufficiently large charge densities at a strontium titanate surface to generate superconductivity (K. Ueno et al. Nature Mater. 7, 855–858; 2008). This has been seen before in doped strontium titanate, but the electrolytic capacitor approach avoids the disorder inherent in doping.

By using mobile ions in an electrolyte to attract charges in the sample, this quirky capacitor can build up charge densities approaching those of chemically doped electronic materials such as high-temperature superconductors. This opens up the possibility of transistor-like devices that can work with very low voltages.

Posted by Anna Petherick at 04:27 PM | Permalink | Comments (0) | TrackBacks (0)