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ScienceWeek
SCIENCEWEEK
June 1, 2007
Vol. 11 - Number 21
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Aristotle has said that the sweetest of all things is knowledge. And he is right. But if you were to suppose that the _publication_ of a new view were productive of unbounded sweetness, you would be mightily mistaken. No one who disturbs his fellow men with a new view remains unpunished.
-- Ernst Mach (1838-1916)
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Contents (full text below):
1. Anthropology: Walking on Trees
2. Physics: Watching Electrons Break Up
3. Ageing: When Less Is More
4. Evolutionary Biology: Animal Personalities
5. Protein Science: Discriminating Taste of Prions
6. Astrophysics: Water Worlds in the Making
7. Parkinson's Disease and Pesticide Exposures
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1.
Science 1 June 2007: Vol. 316. no. 5829, pp. 1292 - 1294 DOI: 10.1126/science.1143571
Anthropology: Walking on Trees
Paul O'Higgins and Sarah Elton
For decades, researchers have viewed standing upright and walking on the ground on two legs as defining features of the hominins (humans and our closest extinct relatives). However, we are beginning to learn that some apes in the Miocene (5 to 23 million years ago) not only had upright postures (1) but also incorporated bipedalism into their motion (2, 3). Such movement may well have occurred in the trees. This raises the possibility that preadaptations for hominin bipedalism arose in arboreal settings rather than in terrestrial environments. On page 1328 of this issue, Thorpe and colleagues present compelling new evidence in support of this theory (4). Using observational data from modern orangutans, they argue that hominin bipedal walking is not novel but rather a development of locomotor behaviors already established in the ancestor of great apes.
In modern orangutans, hand-assisted bipedalism with extended lower limbs in the small branches of the forest canopy allows movement on slender, springy supports. This enables the orangutans to access resources in the forest canopy that would otherwise be difficult to procure, or to cross between trees with minimum energy expenditure. These advantages might well have provided sufficient selective pressure for bipedal adaptations in arboreal habitats.
The orangutan model provides three scenarios for the emergence of modern great ape and human locomotor strategies from hand-assisted, straight-lower-limbed, arboreal bipedalism (see the figure). In the first, forest canopy fragmentation during the Miocene of Africa led to increased vertical climbing, rather than always crossing from tree to tree at canopy level. Thorpe et al. suggest that this climbing behavior, which is similar to knuckle walking, predisposed gorilla and chimpanzee ancestors to the independent acquisition of forms of knuckle walking. In the second scenario, orangutan ancestors in Southeast Asia became even more specialized in traversing, at canopy level, the shrinking closed-canopy forest. Finally, hominins retained and further adapted preexisting arboreal bipedalism to exploit emerging, more open terrain between forested areas. This third scenario is consistent with the long forelimbs that are found in association with obviously bipedally adapted hindlimbs in various early hominins.
It is necessary in a model such as this to simplify the nature and tempo of environmental change, although Thorpe and colleagues do point out the probable fluctuations in forest coverage that occurred during the Miocene. Inevitably, past environments were complex, and there was no straightforward transition from forested to more open habitats. Primate adaptations and radiations were equally complex, and it has been argued (5) that apes diversified into a variety of environments well before any substantial Miocene forest shrinkage. Nonetheless, locomotion is strongly tied to habitat and therefore evolves in response to external pressures, whether they are caused by environmental change or by niche differentiation.
The work of Thorpe et al. reopens the debate about the origins of our own peculiar commitment to bipedal locomotion. To date, there is no consensus about the adaptive scenario that could have led to the adoption of terrestrial bipedalism. Many theories have been proposed, including the postural feeding hypothesis (6); a model (7) attributing bipedality to the social, sexual, and reproductive behavior of early hominins, in which bipedalism allowed better provisioning of offspring and enhanced reproductive fitness; the thermoregulatory hypothesis (8), where standing upright on two legs is argued to reduce the amount of the body directly exposed to sunlight, therefore allowing foraging during the hottest part of the day; and the appeasement model (9), which focuses on bipedal displays that allow for the relatively peaceful resolution of conflicts.
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2.
Science 1 June 2007: Vol. 316. no. 5829, pp. 1290 - 1291 DOI: 10.1126/science.1143504
Physics: Watching Electrons Break Up
Piers Coleman
Electrons are surprisingly rugged particles that fiercely maintain their identity in metals. As they move, they conduct heat and electric charge in all directions in a precisely fixed ratio, a universal property of electricity called the Wiedemann-Franz law. On page 1320 of this issue, Tanatar et al. (1) show that under the right conditions, metals can exhibit a new type of electrical conductivity for which the Wiedemann-Franz law no longer holds. Under these conditions, conventional electrons appear to live alongside a fundamentally different kind of electricity in which electrons have broken apart and reformed into a new class of charge- and heat-carrying excitation. Such failures of accepted laws in science often signal new and interesting underlying causes, and these results may help us understand the mechanisms behind high-temperature superconductors and other unusual materials.
In the 19th century, physicists empirically discovered two important laws governing the thermal and electrical properties of dense matter: the Dulong-Petit law and the Wiedemann-Franz law. At that time, most scientists believed that Dulong and Petit's law, stating that the specific heat of all materials is a constant, was a fundamental law of nature. Yet it was the failure of the Dulong-Petit law at low temperatures in the 20th century that helped to usher in the era of quantum mechanics (2). Early on, physicists did not understand the mechanisms behind the Wiedemann-Franz law, yet it went on to survive, and we know it now to be a consequence of the discrete, quantum nature of electrons in electrical current.
In a normal metal, the quantum motion of electrons is very highly organized (see the left panel of the figure) and might be likened to the organization of aircraft traffic near a major airport. Just as airplanes are stacked by altitude, each in its own slot, electrons are tightly stacked in velocity up to a maximum value called the Fermi velocity. Electron traffic is controlled by quantum physics and the "Pauli exclusion principle," which prevents more than two electrons per velocity slot and helps electrons protect their identity, even as they jostle one another inside the electron cloud. As long as this organization holds, the Wiedemann-Franz law is expected to remain intact.
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3.
Nature 447, 536-537 (31 May 2007) | doi:10.1038/447536a; Published online 30 May 2007
Ageing: When Less Is More
Adam Antebi
Restricting dietary intake is one way to promote longevity. The identification of two genes that specifically mediate this effect in worms provides insight into the molecular mechanisms underlying ageing.
Dietary restriction -- a reduction of food intake by 40–60% without malnutrition -- has remarkable benefits for health and lifespan, extending the survival of species as diverse as yeast, worms, flies, rodents and perhaps even primates. Yet despite intensive study, the molecular basis of the effects of dietary restriction in animals has remained largely elusive. Elsewhere in this issue, two groups1, 2 report a role for a pair of evolutionarily conserved proteins -- PHA-4 and SKN-1 -- in conferring extended survival under dietary restriction in the small roundworm Caenorhabditis elegans. Both PHA-4 and SKN-1 are transcription factors, regulating the expression of many genes. Moreover, evidence suggests that they may also trigger hormones that coordinate physiological responses to dietary restriction.
Restricting dietary intake in worms can be achieved by diluting their bacterial food. At optimum conditions for dietary-restriction-induced longevity, worms typically live 20–50% longer than fully fed animals. The PHA-4 protein, which was originally described for its role in specifying the pharynx in worm embryos, is a member of the forkhead family of transcription factors, and is very similar to mammalian FOXA proteins3, 4. In mammals, FOXA proteins have developmental roles, and regulate glucose metabolism later in life5. In C. elegans, PHA-4 is present from embryo to adult, but its functions in later life were largely unknown.
To examine PHA-4 function in adult worms, Panowski and colleagues (page 550)1 used genetic manipulations to inactivate the pha-4 gene in adult worms, without affecting its embryonic activity. Intriguingly, they found that pha-4 mutants did not respond to dietary manipulations, showing a similar median adult lifespan at all tested food concentrations; however, other processes such as food ingestion and feeding behaviour appeared normal. By inference, therefore, PHA-4 function in adult worms is to respond to dietary changes, and to increase survival under conditions of dietary restriction.
The authors also found that the requirement for PHA-4 was very specific. Systematic knockdown of the other 14 forkhead transcription factors expressed in the worm — including DAF-16/FOXO — had little effect on longevity induced by restricting dietary intake. The DAF-16/FOXO transcription factor works in another well-known longevity pathway — that of insulin/IGF signalling, which dramatically influences lifespan in worms, flies and mice6. A modest reduction of insulin/IGF signalling activates DAF-16/FOXO, which mediates a twofold extension of worm lifespan. Similarly, inactivation of DAF-16 completely abolishes insulin/IGF-signalling-mediated longevity6.
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4.
Nature 447, 539-540 (31 May 2007) | doi:10.1038/447539a; Published online 30 May 2007
Evolutionary Biology: Animal Personalities
Alison M. Bell
That different people differ in their readiness to take risks is an obvious feature of human personality. Theoretical advances now help in making sense of observations of analogous behaviour in animals.
Personality might seem to require a complexity and subtlety that is unique to humans. But evidence for individual variation in traits that we would recognize as personality, for example aggressiveness in fighting or boldness in the face of a predator, has cropped up in animals ranging from fish to monkeys to squid. Even an individual spider behaves differently from other spiders, through time and in different situations1. Wolf et al. (page 581 of this issue2) now show how such variation in behaviour can make evolutionary sense.
Personality has been difficult to explain from an evolutionary perspective because, at first glance, it could seem maladaptive3. An individual that is consistently uninhibited and bold is going to end up eaten by a predator. The optimal animal should be bold only when it makes sense to be bold, and adjust its behaviour when the situation changes. Although animals are legendary for their remarkable 'behavioural plasticity' (think migration or camouflage, for example), there is growing evidence that animals do not always change their behaviour as much as they should. In other words, behavioural plasticity is limited3.
One possible explanation for this is that individuals should behave consistently if it's simply too hard to undergo a personality transformation. If turning off a general tendency to be aggressive requires time and energy to entirely rewire neural machinery, or to build a physiology that can support a different metabolism, then individuals might be better off sticking to an intermediate strategy4. Similarly, if information about the immediate environment is uncertain, then it makes sense just to behave the same way and avoid the risk of making a mistake5.
This line of reasoning can help to explain why a given individual behaves consistently, but not, for example, why some individuals are always more aggressive than others. Such variation is puzzling, because natural selection will favour individuals with characteristics that perform the best, and less 'fit' individuals will be removed from the population. If a trait is heritable and linked to survival or reproductive success, then evolutionary theory tells us that variation will eventually disappear from the population. But, empirically, we know that personality traits are heritable6, are linked to fitness7 and are quite variable.
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5.
Nature 447, 541-542 (31 May 2007) | doi:10.1038/447541b; Published online 30 May 2007
Protein Science: Discriminating Taste of Prions
Witold K. Surewicz
Prions are infectious proteins that are involved in brain-wasting disorders such as mad cow disease. In yeast, specific sequences of amino acids in prions seem to mediate prion propagation and cross-species transmissibility.
Few diseases have generated as much interest and controversy in recent years as transmissible spongiform encephalopathies (TSEs) — a group of fatal neurodegenerative disorders that includes Creutzfeldt–Jakob disease in humans and 'mad cow' disease1, 2. The protein-only hypothesis of TSE propagation postulates that the infectious pathogen, called a prion, is devoid of the nucleic acids that comprise genes, and is an abnormally shaped version of the normal prion protein, a naturally occurring molecule of unknown function. The infectious prion replicates by binding to its host's normal prion protein and forcing it to take on the abnormal conformation1. Once heretical, this notion that proteins alone can be infectious is now rapidly gaining acceptance. Paradoxically, the most compelling evidence for this idea has come not from studying TSEs, but from prion-like entities in yeast and other fungi3, 4, 5, 6. In this issue (page 556), Tessier and Lindquist7 present intriguing findings that clarify many of the mechanisms underlying the conversion of yeast prion proteins to an infectious form.
Whereas mammalian prions cause a dreaded brain-wasting disease, infectious prions in yeast change the behaviour (or phenotype) of these simple organisms, with the altered characteristics passing from one generation to the next3, 4. Thus, yeast prions act as protein-only 'genes'. The most extensively studied yeast prion protein is called Sup35, which, when conformationally modified into an infectious prion, leads to a yeast phenotype that is defective in terminating protein synthesis. The conversion of Sup35, and other yeast prions, to the infectious state is associated with their polymerization into amyloid fibrils — highly organized, thread-like aggregates that are also linked to Alzheimer's disease and other 'protein-misfolding' disorders3, 4.
To investigate the precise mechanisms underlying prion conversion, Tessier and Lindquist7 synthesized a large library of overlapping peptides derived from the amino-acid sequences of two regions of Sup35 — its N-terminal (N) and its middle (M) regions, jointly denoted ScNM — from the budding yeast Saccharomyces cerevisiae. They then used an array assay to analyse the ability of these sequences to bind to and modify the full-length protein (Fig. 1). They found that only a tiny subset of ScNM peptides could capture the ScNM protein from solution, and that these peptides selectively promoted the assembly of amyloid fibrils. The authors conclude that small elements of the Sup35 amino-acid sequence can recognize soluble conformations of the protein with unusual specificity, and that this is sufficient to drive the conversion of soluble proteins to the abnormal prion state.
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6.
Nature 447, 535-536 (31 May 2007) | doi:10.1038/447535a; Published online 30 May 2007
Astrophysics: Water Worlds in the Making
Roy van Boekel
Meticulous observations of the disk of gas and dust around one young star seem to imply icy, comet-like bodies in the disk's inner regions. Could these be the building-blocks of water-rich planets like Earth?
The disks of dust and gas around newborn stars provide a natural laboratory for studying the formation of planetary systems. But even the nearest young stars are so far away that conventional telescopes lack the sharpness of vision to see into the very centre of the disk, where habitable planets such as Earth could form. Using the Keck Interferometer — a system of two telescopes on the summit of Mauna Kea, Hawaii — J. A. Eisner has zoomed in on this 'terrestrial region' around one young star. The results1 can be found on page 562. He measures the disk geometry on scales of less than one astronomical unit (AU) — the distance from Earth to the Sun — and directly locates hydrogen gas plunging onto the star. He finds water, too, in the inner disk, arguably stemming from evaporating icy bodies that might even now be forming water-rich, Earth-like planets.
The disks around stars consist mostly of hydrogen gas, but they also contain molecules such as carbon monoxide (CO) and water that are much less abundant, but easier to detect by virtue of their much stronger spectral signatures. About 1% of the disk mass consists of tiny particles of solid material. Put enough of this 'dust' together, and you can make a rocky planet like Earth, or the core of one of the giant gas planets found farther out in our Solar System.
Of the more than 200 'exoplanets' now known to be orbiting stars other than the Sun, a preponderance are giant gas planets close to their parent star. That is partly because these planets are easiest (or rather, least difficult) to detect. Even so, it seems that our Solar System's architecture, which is apparently so favourable for the development of life — rocky planets close to the star, gas giants farther away, all on approximately circular orbits — is not common2. But exactly how uncommon is it?
To find out, we need to go back to the planetary cradle. In most of a circumstellar disk, gas and dust are mixed. In the region of interest close to the star, however, the temperature is so high that solid material vaporizes, and hot gas swirls its way towards the star. Dynamical interactions between this hot gas and forming planets, which cause planets to migrate through the disk, are considered crucial in determining the final architecture of a planetary system3.
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7.
British Medical Bulletin 2006 79-80(1):219-231; doi:10.1093/bmb/ldl018
Parkinson's Disease and Pesticide Exposures
Finlay D. Dick
Introduction: Idiopathic Parkinson's disease (PD) is a neurodegenerative disorder in which loss of dopaminergic neurons in the basal ganglia leads to tremor, bradykinesia, rigidity and postural instability.
Methods: Literature search using Medline
Results: Many studies have found an association between pesticides and PD, but no one agent has been consistently identified. Those implicated include organochlorine insecticides, maneb and paraquat. One meta-analysis of pesticide exposure and PD found an almost doubling of risk in those exposed. Associations with specific agents may be confounded by exposure to other pesticides, making it difficult to identify the causative agent.
Conclusions: The available evidence indicates that pesticides are associated with PD, but further research is needed to identify long-term biomarkers of exposure, improve methods for estimating pesticide-exposure and undertake prospective cohort studies of pesticide-exposed workers.
Parkinson's disease (PD) is a movement disorder, which develops as a consequence of degeneration of the dopaminergic neurons within the basal ganglia. The disease becomes clinically apparent once ~70% of the dopaminergic neurons of the substantia nigra are lost. Neuropathologically, Lewy bodies are typical of PD, although these intra-cytoplasmic neuronal inclusions, which contain {alpha}-synuclein, may be found in other conditions such as dementia with Lewy bodies. PD is principally a disease of ageing, with a peak age of onset of 65 years, although both young onset PD, generally defined as disease onset <40 years, and a rare juvenile form occur.
PD presents with resting tremor, slow movements (bradykinesia) and rigidity and, later, postural instability occurs. Almost half of PD sufferers show asymmetry with signs and symptoms being more marked on one side of the body. The condition was first described by Parkinson,1 an English surgeon, in 1817 in his classic monograph ‘an essay on the shaking palsy’. He described the main features of what is now known as PD and gave case histories of six sufferers, one of whom was a gardener (case I).
The reported incidence of PD varies across the world,2 although whether this reflects genuine differences in disease incidence or better case ascertainment in North American and Western European populations is less clear. There is some evidence to suggest that PD is commoner in Caucasians than Chinese, although this may reflect differing environmental exposures rather than greater genetic susceptibility to the disease.
The diagnosis of PD is essentially a clinical one, but diagnosis can be difficult and other causes of parkinsonism should be considered. Vascular parkinsonism, due to cerebral infarcts, may be confused with PD, but the stepwise progression typical of vascular parkinsonism together with a failure to respond to L-dopa should alert the treating clinician to the correct diagnosis. Patients treated with major tranquilizers or anti-emetics may develop drug-induced parkinsonism but this should be distinguished from PD. Post-mortem studies in the early 1990s found that 24% of patients clinically thought to have had PD actually had another condition (e.g. progressive supra-nuclear palsy or multi-system atrophy). More recently, the diagnostic accuracy of PD, at least among movement disorder specialists, has improved to 90%.3 Diagnostic imprecision has implications for research into the causes of PD, especially when considering studies carried out before the early 1990s, as studies that included a significant proportion of people with parkinsonism rather than PD would have had reduced statistical power to detect associations.
A number of different clinical diagnostic criteria for PD have been published, including the Ward and Gibb criteria, the Gelb criteria and the UK Parkinson's Disease Society (PDS) Brain Bank clinical diagnostic criteria.4 Of these, the most widely used have been the three-step UK PDS Brain Bank criteria: step 1 requires the presence of bradykinesia and at least one of muscular rigidity, 4–6 Hz rest tremor and postural instability; step 2 lists 16 exclusion criteria including a history of definite encephalitis and step 3 lists eight supportive criteria, at least three of which are required for a diagnosis of definite PD.
Genetic research has identified a number of rare familial forms of PD because of single gene mutations.5 These breakthroughs have given researchers valuable new insights into some of the mechanisms that may underlie PD, but nonetheless most cases of PD remain unexplained. Two large twin studies6,7 failed to find evidence of a significant genetic contribution to the burden of typical PD, although in one study,6 genetic factors did seem to make a contribution in younger onset PD (defined in that study as onset <50 years of age).
The generally held view is that PD is due to both environmental and genetic factors and that it is not one disease but rather a number of phenotypically similar conditions.
Studies of environmental risk factors for PD received a fillip following reports of parkinsonism in a small number of drug abusers who had consumed a synthetic opiate, 1-methy-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).8 MPTP is metabolized to the neurotoxin 1-methyl-4-phenylpyridinium (MPP+), which was originally developed as the herbicide, cyperquat. The chemical structure of MPP+ is similar to the widely used bipyridinium herbicide paraquat. This finding prompted a number of epidemiological studies of the association between pesticide exposure and PD.
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