Nonlinear grassland responses to past and future atmospheric CO(2)

Carbon sequestration in soil organic matter may moderate increases in atmospheric CO(2) concentrations (C(a)) as C(a) increases to more than 500 micromol mol(-1) this century from interglacial levels of less than 200 micromol mol(-1) (refs 1 6). However, such carbon storage depends on feedbacks between plant responses to C(a) and nutrient availability. Here we present evidence that soil carbon storage and nitrogen cycling in a grassland ecosystem are much more responsive to increases in past C(a) than to those forecast for the coming century. Along a continuous gradient of 200 to 550 micromol mol(-1) (refs 9, 10), increased C(a) promoted higher photosynthetic rates and altered plant tissue chemistry. Soil carbon was lost at subambient C(a), but was unchanged at elevated C(a) where losses of old soil carbon offset increases in new carbon. Along the experimental gradient in C(a) there was a nonlinear, threefold decrease in nitrogen availability. The differences in sensitivity of carbon storage to historical and future C(a) and increased nutrient limitation suggest that the passive sequestration of carbon in soils may have been important historically, but the ability of soils to continue as sinks is limited.     

Intense equatorial flux spots on the surface of the Earth's core

A large number of high-accuracy vector measurements of the Earth's magnetic field have recently become available from the satellite Oersted, complementing previous vector data from the satellite Magsat, which operated in 1979/80. These data can be used to infer the morphology of the magnetic field at the surface of the fluid core, approximately 2,900 km below the Earth's surface. Here I apply a new methodology to these data to calculate maps of the magnetic field at the core surface which show intense flux spots in equatorial regions. The intensity of these features is unusually large--some have intensities comparable to high-latitude flux patches near the poles, previously identified as the major component of the dynamo field. The tendency for pairing of some of these spots to the north and south of the geographical equator suggests they might be associated with the tops of equatorially symmetric columnar structures in the fluid, or their antisymmetric equivalents. The drift of the equatorial features may represent material flow or could represent wave motion; discrimination of these two effects based on future data could provide new information on the strength of the hidden toroidal magnetic field of the Earth.     

The genome sequence of Bacillus anthracis Ames and comparison to closely related bacteria

Bacillus anthracis is an endospore-forming bacterium that causes inhalational anthrax. Key virulence genes are found on plasmids (extra-chromosomal, circular, double-stranded DNA molecules) pXO1 (ref. 2) and pXO2 (ref. 3). To identify additional genes that might contribute to virulence, we analysed the complete sequence of the chromosome of B. anthracis Ames (about 5.23 megabases). We found several chromosomally encoded proteins that may contribute to pathogenicity--including haemolysins, phospholipases and iron acquisition functions--and identified numerous surface proteins that might be important targets for vaccines and drugs. Almost all these putative chromosomal virulence and surface proteins have homologues in Bacillus cereus, highlighting the similarity of B. anthracis to near-neighbours that are not associated with anthrax. By performing a comparative genome hybridization of 19 B. cereus and Bacillus thuringiensis strains against a B. anthracis DNA microarray, we confirmed the general similarity of chromosomal genes among this group of close relatives. However, we found that the gene sequences of pXO1 and pXO2 were more variable between strains, suggesting plasmid mobility in the group. The complete sequence of B. anthracis is a step towards a better understanding of anthrax pathogenesis.     

Disruption of Cnp1 uncouples oligodendroglial functions in axonal support and myelination

Myelination of axons by oligodendrocytes enables rapid impulse propagation in the central nervous system. But long-term interactions between axons and their myelin sheaths are poorly understood. Here we show that Cnp1, which encodes 2',3'-cyclic nucleotide phosphodiesterase in oligodendrocytes, is essential for axonal survival but not for myelin assembly. In the absence of glial cyclic nucleotide phosphodiesterase, mice developed axonal swellings and neurodegeneration throughout the brain, leading to hydrocephalus and premature death. But, in contrast to previously studied myelin mutants, the ultrastructure, periodicity and physical stability of myelin were not altered in these mice. Genetically, the chief function of glia in supporting axonal integrity can thus be completely uncoupled from its function in maintaining compact myelin. Oligodendrocyte dysfunction, such as that in multiple sclerosis lesions, may suffice to cause secondary axonal loss.     

Deposition of 1.88-billion-year-old iron formations as a consequence of rapid crustal growth

Iron formations are chemical sedimentary rocks comprising layers of iron-rich and silica-rich minerals whose deposition requires anoxic and iron-rich (ferruginous) sea water. Their demise after the rise in atmospheric oxygen by 2.32?billion years (Gyr) ago has been attributed to the removal of dissolved iron through progressive oxidation or sulphidation of the deep ocean. Therefore, a sudden return of voluminous iron formations nearly 500?million years later poses an apparent conundrum. Most late Palaeoproterozoic iron formations are about 1.88?Gyr old and occur in the Superior region of North America. Major iron formations are also preserved in Australia, but these were apparently deposited after the transition to a sulphidic ocean at 1.84?Gyr ago that should have terminated iron formation deposition, implying that they reflect local marine conditions. Here we date zircons in tuff layers to show that iron formations in the Frere Formation of Western Australia are about 1.88?Gyr old, indicating that the deposition of iron formations from two disparate cratons was coeval and probably reflects global ocean chemistry. The sudden reappearance of major iron formations at 1.88?Gyr ago--contemporaneous with peaks in global mafic-ultramafic magmatism, juvenile continental and oceanic crust formation, mantle depletion and volcanogenic massive sulphide formation--suggests deposition of iron formations as a consequence of major mantle activity and rapid crustal growth. Our findings support the idea that enhanced submarine volcanism and hydrothermal activity linked to a peak in mantle melting released large volumes of ferrous iron and other reductants that overwhelmed the sulphate and oxygen reservoirs of the ocean, decoupling atmospheric and seawater redox states, and causing the return of widespread ferruginous conditions. Iron formations formed on clastic-starved coastal shelves where dissolved iron upwelled and mixed with oxygenated surface water. The disappearance of iron formations after this event may reflect waning mafic-ultramafic magmatism and a diminished flux of hydrothermal iron relative to seawater oxidants.     

Cardiac angiogenic imbalance leads to peripartum cardiomyopathy

Peripartum cardiomyopathy (PPCM) is an often fatal disease that affects pregnant women who are near delivery, and it occurs more frequently in women with pre-eclampsia and/or multiple gestation. The aetiology of PPCM, and why it is associated with pre-eclampsia, remain unknown. Here we show that PPCM is associated with a systemic angiogenic imbalance, accentuated by pre-eclampsia. Mice that lack cardiac PGC-1α, a powerful regulator of angiogenesis, develop profound PPCM. Importantly, the PPCM is entirely rescued by pro-angiogenic therapies. In humans, the placenta in late gestation secretes VEGF inhibitors like soluble FLT1 (sFLT1), and this is accentuated by multiple gestation and pre-eclampsia. This anti-angiogenic environment is accompanied by subclinical cardiac dysfunction, the extent of which correlates with circulating levels of sFLT1. Exogenous sFLT1 alone caused diastolic dysfunction in wild-type mice, and profound systolic dysfunction in mice lacking cardiac PGC-1α. Finally, plasma samples from women with PPCM contained abnormally high levels of sFLT1. These data indicate that PPCM is mainly a vascular disease, caused by excess anti-angiogenic signalling in the peripartum period. The data also explain how late pregnancy poses a threat to cardiac homeostasis, and why pre-eclampsia and multiple gestation are important risk factors for the development of PPCM.