Fitness reduction associated with the deletion of a satellite DNA array

Satellite DNA refers to a class of tandem repeats of very simple sequences, usually A + T or G + C rich, which form a satellite band on a CsCl gradient. Their ubiquity and abundance in higher eukaryotes have led to speculation about their functions. It has often been suggested that satellite DNAs are merely innocuous genetic parasites or comprise 'junk' DNA. The recent identification of an array of satellite DNA repeats as the Responder (Rsp) locus of Drosophila melanogaster provides a new perspective on these elements. Rsp is in the centromeric heterochromatin of most natural second chromosomes. It causes spermatids bearing it to degenerate after meiosis when the homologous second chromosome is a Segregation Distorter (SD) chromosome. That is, SD targets the Rsp locus on its homologue for destruction during spermatogenesis, causing meiotic drive. Why then does the Rsp locus, a large array of satellite repeats, exist at all? One plausible explanation is that its existence contributes to the fitness of flies bearing it, compensating for the loss through meiotic drive. A direct demonstration of the usefulness of any family of satellite DNA is to compare the fitnesses of individuals with and without it. Previously, such an experiment has been difficult because the absence of a characteristic phenotype has precluded an efficient selection of deletion mutations. In this report we attempt to demonstrate a fitness reduction associated with the deletion of Rsp satellite DNA as well as the life stages at which such a reduction occurs.     

Triplet-singlet spin relaxation via nuclei in a double quantum dot

The spin of a confined electron, when oriented originally in some direction, will lose memory of that orientation after some time. Physical mechanisms leading to this relaxation of spin memory typically involve either coupling of the electron spin to its orbital motion or to nuclear spins. Relaxation of confined electron spin has been previously measured only for Zeeman or exchange split spin states, where spin-orbit effects dominate relaxation; spin flips due to nuclei have been observed in optical spectroscopy studies. Using an isolated GaAs double quantum dot defined by electrostatic gates and direct time domain measurements, we investigate in detail spin relaxation for arbitrary splitting of spin states. Here we show that electron spin flips are dominated by nuclear interactions and are slowed by several orders of magnitude when a magnetic field of a few millitesla is applied. These results have significant implications for spin-based information processing.     

Lightning-induced intensification of the ionospheric sporadic E layer

A connection between thunderstorms and the ionosphere has been hypothesized since the mid-1920s. Several mechanisms have been proposed to explain this connection, and evidence from modelling as well as various types of measurements demonstrate that lightning can interact with the lower ionosphere. It has been proposed, on the basis of a few observed events, that the ionospheric 'sporadic E' layer--transient, localized patches of relatively high electron density in the mid-ionosphere E layer, which significantly affect radio-wave propagation--can be modulated by thunderstorms, but a more formal statistical analysis is still needed. Here we identify a statistically significant intensification and descent in altitude of the mid-latitude sporadic E layer directly above thunderstorms. Because no ionospheric response to low-pressure systems without lightning is detected, we conclude that this localized intensification of the sporadic E layer can be attributed to lightning. We suggest that the co-location of lightning and ionospheric enhancement can be explained by either vertically propagating gravity waves that transfer energy from the site of lightning into the ionosphere, or vertical electrical discharge, or by a combination of these two mechanisms.     

Upwelling-driven nearshore hypoxia signals ecosystem and oceanographic changes in the northeast Pacific

Seasonal development of dissolved-oxygen deficits (hypoxia) represents an acute system-level perturbation to ecological dynamics and fishery sustainability in coastal ecosystems around the globe. Whereas anthropogenic nutrient loading has increased the frequency and severity of hypoxia in estuaries and semi-enclosed seas, the occurrence of hypoxia in open-coast upwelling systems reflects ocean conditions that control the delivery of oxygen-poor and nutrient-rich deep water onto continental shelves. Upwelling systems support a large proportion of the world's fisheries, therefore understanding the links between changes in ocean climate, upwelling-driven hypoxia and ecological perturbations is critical. Here we report on the unprecedented development of severe inner-shelf (<70 m) hypoxia and resultant mass die-offs of fish and invertebrates within the California Current System. In 2002, cross-shelf transects revealed the development of abnormally low dissolved-oxygen levels as a response to anomalously strong flow of subarctic water into the California Current System. Our findings highlight the sensitivity of inner-shelf ecosystems to variation in ocean conditions, and the potential impacts of climate change on marine communities.     

Essential role for the p110delta phosphoinositide 3-kinase in the allergic response

Inflammatory substances released by mast cells induce and maintain the allergic response. Mast cell differentiation and activation are regulated, respectively, by stem cell factor (SCF; also known as Kit ligand) and by allergen in complex with allergen-specific immunoglobulin E (IgE). Activated SCF receptors and high-affinity receptors for IgE (FcvarepsilonRI) engage phosphoinositide 3-kinases (PI(3)Ks) to generate intracellular lipid second messenger signals. Here, we report that genetic or pharmacological inactivation of the p110delta isoform of PI(3)K in mast cells leads to defective SCF-mediated in vitro proliferation, adhesion and migration, and to impaired allergen-IgE-induced degranulation and cytokine release. Inactivation of p110delta protects mice against anaphylactic allergic responses. These results identify p110delta as a new target for therapeutic intervention in allergy and mast-cell-related pathologies.