Competence to replicate in the unfertilized egg is conferred by Cdc6 during meiotic maturation

Meiotic maturation, the final step of oogenesis, is a crucial stage of development in which an immature oocyte becomes a fertilizable egg. In Xenopus, the ability to replicate DNA is acquired during maturation at breakdown of the nuclear envelope by translation of a DNA synthesis inducer that is not present in the oocyte. Here we identify Cdc6, which is essential for recruiting the minichromosome maintenance (MCM) helicase to the pre-replication complex, as this inducer of DNA synthesis. We show that maternal cdc6 mRNA but not protein is stored in the oocyte. Cdc6 protein is synthesized during maturation, but this process can be blocked by degrading the maternal cdc6 mRNA by oligonucleotide antisense injections or by translation inhibition. Rescue experiments using recombinant Cdc6 protein show that Cdc6 is the only missing replication factor whose translation is necessary and sufficient to confer DNA replication competence to the egg before fertilization. The licence to replicate is given by Cdc6 at the end of meiosis I, but the cytostatic factor (CSF) pathway, which maintains large amounts of active Cdc2/Cyclin B2, prevents the entry into S phase until fertilization.     

Angiotensin-converting enzyme 2 is an essential regulator of heart function

Cardiovascular diseases are predicted to be the most common cause of death worldwide by 2020. Here we show that angiotensin-converting enzyme 2 (ace2) maps to a defined quantitative trait locus (QTL) on the X chromosome in three different rat models of hypertension. In all hypertensive rat strains, ACE2 messenger RNA and protein expression were markedly reduced, suggesting that ace2 is a candidate gene for this QTL. Targeted disruption of ACE2 in mice results in a severe cardiac contractility defect, increased angiotensin II levels, and upregulation of hypoxia-induced genes in the heart. Genetic ablation of ACE on an ACE2 mutant background completely rescues the cardiac phenotype. But disruption of ACER, a Drosophila ACE2 homologue, results in a severe defect of heart morphogenesis. These genetic data for ACE2 show that it is an essential regulator of heart function in vivo.     

Mid-mantle deformation inferred from seismic anisotropy

With time, convective processes in the Earth's mantle will tend to align crystals, grains and inclusions. This mantle fabric is detectable seismologically, as it produces an anisotropy in material properties--in particular, a directional dependence in seismic-wave velocity. This alignment is enhanced at the boundaries of the mantle where there are rapid changes in the direction and magnitude of mantle flow, and therefore most observations of anisotropy are confined to the uppermost mantle or lithosphere and the lowermost-mantle analogue of the lithosphere, the D" region. Here we present evidence from shear-wave splitting measurements for mid-mantle anisotropy in the vicinity of the 660-km discontinuity, the boundary between the upper and lower mantle. Deep-focus earthquakes in the Tonga-Kermadec and New Hebrides subduction zones recorded at Australian seismograph stations record some of the largest values of shear-wave splitting hitherto reported. The results suggest that, at least locally, there may exist a mid-mantle boundary layer, which could indicate the impediment of flow between the upper and lower mantle in this region.     

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.     

Coprophagy: an unusual source of essential carotenoids

The rare Egyptian vulture (Neophron percnopterus) stands out among the Old World vultures (Family Accipitridae) because of its brightly ornamented head, which is coloured yellow by carotenoid pigments, and its practice of feeding on faeces. Here we show that Egyptian vultures obtain these pigments from the excrement of ungulates. To our knowledge, this is the first demonstration that faeces can be used as a source of carotenoids by a vertebrate.     

Spatial scale dictates the productivity-biodiversity relationship

The diversity of life is heterogeneously distributed across the Earth. A primary cause for this pattern is the heterogeneity in the amount of energy, or primary productivity (the rate of carbon fixed through photosynthesis), available to the biota in a given location. But the shape of the relationship between productivity and species diversity is highly variable. In many cases, the relationship is 'hump-shaped', where diversity peaks at intermediate productivity. In other cases, diversity increases linearly with productivity. A possible reason for this discrepancy is that data are often collected at different spatial scales. If the mechanisms that determine species diversity vary with spatial scale, then so would the shape of the productivity-diversity relationship. Here, we present evidence for scale-dependent productivity-diversity patterns in ponds. When the data were viewed at a local scale (among ponds), the relationship was hump-shaped, whereas when the same data were viewed at a regional scale (among watersheds), the relationship was positively linear. This dependence on scale results because dissimilarity in local species composition within regions increased with productivity.     

Biodiversity as a barrier to ecological invasion

Biological invasions are a pervasive and costly environmental problem that has been the focus of intense management and research activities over the past half century. Yet accurate predictions of community susceptibility to invasion remain elusive. The diversity resistance hypothesis, which argues that diverse communities are highly competitive and readily resist invasion, is supported by both theory and experimental studies conducted at small spatial scales. However, there is also convincing evidence that the relationship between the diversity of native and invading species is positive when measured at regional scales. Although this latter relationship may arise from extrinsic factors, such as resource heterogeneity, that covary with diversity of native and invading species at large scales, the mechanisms conferring greater invasion resistance to diverse communities at local scales remain unknown. Using neighbourhood analyses, a technique from plant competition studies, we show here that species diversity in small experimental grassland plots enhances invasion resistance by increasing crowding and species richness in localized plant neighbourhoods. Both the establishment (number of invaders) and success (proportion of invaders that are large) of invading plants are reduced. These results suggest that local biodiversity represents an important line of defence against the spread of invaders.