Mantle compensation of active metamorphic core complexes at Woodlark rift in Papua New Guinea

In many highly extended rifts on the Earth, tectonic removal of the upper crust exhumes mid-crustal rocks, producing metamorphic core complexes. These structures allow the upper continental crust to accommodate tens of kilometres of extension, but it is not clear how the lower crust and underlying mantle respond. Also, despite removal of the upper crust, such core complexes remain both topographically high and in isostatic equilibrium. Because many core complexes in the western United States are underlain by a flat Moho discontinuity, it has been widely assumed that their elevation is supported by flow in the lower crust or by magmatic underplating. These processes should decouple upper-crust extension from that in the mantle. In contrast, here we present seismic observations of metamorphic core complexes of the western Woodlark rift that show the overall crust to be thinned beneath regions of greatest surface extension. These core complexes are actively being exhumed at a rate of 5-10 km Myr(-1), and the thinning of the underlying crust appears to be compensated by mantle rocks of anomalously low density, as indicated by low seismic velocities. We conclude that, at least in this case, the development of metamorphic core complexes and the accommodation of high extension is not purely a crustal phenomenon, but must involve mantle extension.     

A neural correlate of response bias in monkey caudate nucleus

Primates are equipped with neural circuits in the prefrontal cortex, the parietal cortex and the basal ganglia that predict the availability of reward during the performance of behavioural tasks. It is not known, however, how reward value is incorporated in the control of action. Here we identify neurons in the monkey caudate nucleus that create a spatially selective response bias depending on the expected gain. In behavioural tasks, the monkey had to make a visually guided eye movement in every trial, but was rewarded for a correct response in only half of the trials. Reward availability was predictable on the basis of the spatial position of the visual target. We found that caudate neurons change their discharge rate systematically, even before the appearance of the visual target, and usually fire more when the contralateral position is associated with reward. Strong anticipatory activity of neurons with a contralateral preference is associated with decreased latency for eye movements in the contralateral direction. We conclude that this neuronal mechanism creates an advance bias that favours a spatial response when it is associated with a high reward value.     

Density-dependent mortality and the latitudinal gradient in species diversity

Ecologists have long postulated that density-dependent mortality maintains high tree diversity in the tropics. If species experience greater mortality when abundant, then more rare species can persist. Agents of density-dependent mortality (such as host-specific predators, and pathogens) may be more prevalent or have stronger effects in tropical forests, because they are not limited by climatic factors. If so, decreasing density-dependent mortality with increasing latitude could partially explain the observed latitudinal gradient in tree diversity. This hypothesis has never been tested with latitudinal data. Here we show that several temperate tree species experience density-dependent mortality between seed dispersal and seedling establishment. The proportion of species affected is equivalent to that in tropical forests, failing to support the hypothesis that this mechanism is more prevalent at tropical latitudes. We further show that density-dependent mortality is misinterpreted in previous studies. Our results and evidence from other studies suggest that density-dependent mortality is important in many forests. Thus, unless the strength of density-dependent mortality varies with latitude, this mechanism is not likely to explain the high diversity of tropical forests.     

Biological and biomedical implications of the co-evolution of pathogens and their hosts

Co-evolution between host and pathogen is, in principle, a powerful determinant of the biology and genetics of infection and disease. Yet co-evolution has proven difficult to demonstrate rigorously in practice, and co-evolutionary thinking is only just beginning to inform medical or veterinary research in any meaningful way, even though it can have a major influence on how genetic variation in biomedically important traits is interpreted. Improving our understanding of the biomedical significance of co-evolution will require changing the way in which we look for it, complementing the phenomenological approach traditionally favored by evolutionary biologists with the exploitation of the extensive data becoming available on the molecular biology and molecular genetics of host-pathogen interactions.     

Reduced adaptation of a non-recombining neo-Y chromosome

Sex chromosomes are generally believed to have descended from a pair of homologous autosomes. Suppression of recombination between the ancestral sex chromosomes led to the genetic degeneration of the Y chromosome. In response, the X chromosome may become dosage-compensated. Most proposed mechanisms for the degeneration of Y chromosomes involve the rapid fixation of deleterious mutations on the Y. Alternatively, Y-chromosome degeneration might be a response to a slower rate of adaptive evolution, caused by its lack of recombination. Here we report patterns of DNA polymorphism and divergence at four genes located on the neo-sex chromosomes of Drosophila miranda. We show that a higher rate of protein sequence evolution of the neo-X-linked copy of Cyclin B relative to the neo-Y copy is driven by positive selection, which is consistent with the adaptive hypothesis for the evolution of the Y chromosome. In contrast, the neo-Y-linked copies of even-skipped and roundabout show an elevated rate of protein evolution relative to their neo-X homologues, probably reflecting the reduced effectiveness of selection against deleterious mutations in a non-recombining genome. Our results provide evidence for the importance of sexual recombination for increasing and maintaining the level of adaptation of a population.     

Nitric oxide regulates the heart by spatial confinement of nitric oxide synthase isoforms

Subcellular localization of nitric oxide (NO) synthases with effector molecules is an important regulatory mechanism for NO signalling. In the heart, NO inhibits L-type Ca2+ channels but stimulates sarcoplasmic reticulum (SR) Ca2+ release, leading to variable effects on myocardial contractility. Here we show that spatial confinement of specific NO synthase isoforms regulates this process. Endothelial NO synthase (NOS3) localizes to caveolae, where compartmentalization with beta-adrenergic receptors and L-type Ca2+ channels allows NO to inhibit beta-adrenergic-induced inotropy. Neuronal NO synthase (NOS1), however, is targeted to cardiac SR. NO stimulation of SR Ca2+ release via the ryanodine receptor (RyR) in vitro, suggests that NOS1 has an opposite, facilitative effect on contractility. We demonstrate that NOS1-deficient mice have suppressed inotropic response, whereas NOS3-deficient mice have enhanced contractility, owing to corresponding changes in SR Ca2+ release. Both NOS1-/- and NOS3-/- mice develop age-related hypertrophy, although only NOS3-/- mice are hypertensive. NOS1/3-/- double knockout mice have suppressed beta-adrenergic responses and an additive phenotype of marked ventricular remodelling. Thus, NOS1 and NOS3 mediate independent, and in some cases opposite, effects on cardiac structure and function.