Placing late Neanderthals in a climatic context

Attempts to place Palaeolithic finds within a precise climatic framework are complicated by both uncertainty over the radiocarbon calibration beyond about 21,500 14C years bp and the absence of a master calendar chronology for climate events from reference archives such as Greenland ice cores or speleothems. Here we present an alternative approach, in which 14C dates of interest are mapped directly onto the palaeoclimate record of the Cariaco Basin by means of its 14C series, circumventing calendar age model and correlation uncertainties, and placing dated events in the millennial-scale climate context of the last glacial period. This is applied to different sets of dates from levels with Mousterian artefacts, presumably produced by late Neanderthals, from Gorham's Cave in Gibraltar: first, generally accepted estimates of about 32,000 14C years bp for the uppermost Mousterian levels; second, a possible extended Middle Palaeolithic occupation until about 28,000 14C years bp; and third, more contentious evidence for persistence until about 24,000 14C years bp. This study shows that the three sets translate to different scenarios on the role of climate in Neanderthal extinction. The first two correspond to intervals of general climatic instability between stadials and interstadials that characterized most of the Middle Pleniglacial and are not coeval with Heinrich Events. In contrast, if accepted, the youngest date indicates that late Neanderthals may have persisted up to the onset of a major environmental shift, which included an expansion in global ice volume and an increased latitudinal temperature gradient. More generally, our radiocarbon climatostratigraphic approach can be applied to any 'snapshot' date from discontinuous records in a variety of deposits and can become a powerful tool in evaluating the climatic signature of critical intervals in Late Pleistocene human evolution.     

14-3-3sigma controls mitotic translation to facilitate cytokinesis

14-3-3 proteins are crucial in a wide variety of cellular responses including cell cycle progression, DNA damage checkpoints and apoptosis. One particular 14-3-3 isoform, sigma, is a p53-responsive gene, the function of which is frequently lost in human tumours, including breast and prostate cancers as a result of either hypermethylation of the 14-3-3sigma promoter or induction of an oestrogen-responsive ubiquitin ligase that specifically targets 14-3-3sigma for proteasomal degradation. Loss of 14-3-3sigma protein occurs not only within the tumours themselves but also in the surrounding pre-dysplastic tissue (so-called field cancerization), indicating that 14-3-3sigma might have an important tumour suppressor function that becomes lost early in the process of tumour evolution. The molecular basis for the tumour suppressor function of 14-3-3sigma is unknown. Here we report a previously unknown function for 14-3-3sigma as a regulator of mitotic translation through its direct mitosis-specific binding to a variety of translation/initiation factors, including eukaryotic initiation factor 4B in a stoichiometric manner. Cells lacking 14-3-3sigma, in marked contrast to normal cells, cannot suppress cap-dependent translation and do not stimulate cap-independent translation during and immediately after mitosis. This defective switch in the mechanism of translation results in reduced mitotic-specific expression of the endogenous internal ribosomal entry site (IRES)-dependent form of the cyclin-dependent kinase Cdk11 (p58 PITSLRE), leading to impaired cytokinesis, loss of Polo-like kinase-1 at the midbody, and the accumulation of binucleate cells. The aberrant mitotic phenotype of 14-3-3sigma-depleted cells can be rescued by forced expression of p58 PITSLRE or by extinguishing cap-dependent translation and increasing cap-independent translation during mitosis by using rapamycin. Our findings show how aberrant mitotic translation in the absence of 14-3-3sigma impairs mitotic exit to generate binucleate cells and provides a potential explanation of how 14-3-3sigma-deficient cells may progress on the path to aneuploidy and tumorigenesis.     

Observation of the two-channel Kondo effect

Some of the most intriguing problems in solid-state physics arise when the motion of one electron dramatically affects the motion of surrounding electrons. Traditionally, such highly correlated electron systems have been studied mainly in materials with complex transition metal chemistry. Over the past decade, researchers have learned to confine one or a few electrons within a nanometre-scale semiconductor 'artificial atom', and to understand and control this simple system in detail(3). Here we combine artificial atoms to create a highly correlated electron system within a nano-engineered semiconductor structure. We tune the system in situ through a quantum phase transition between two distinct states, each a version of the Kondo state, in which a bound electron interacts with surrounding mobile electrons. The boundary between these competing Kondo states is a quantum critical point-namely, the exotic and previously elusive two-channel Kondo state, in which electrons in two reservoirs are entangled through their interaction with a single localized spin.     

Abrupt onset of a second energy gap at the superconducting transition of underdoped Bi2212

The superconducting gap--an energy scale tied to the superconducting phenomena--opens on the Fermi surface at the superconducting transition temperature (T(c)) in conventional BCS superconductors. In underdoped high-T(c) superconducting copper oxides, a pseudogap (whose relation to the superconducting gap remains a mystery) develops well above T(c) (refs 1, 2). Whether the pseudogap is a distinct phenomenon or the incoherent continuation of the superconducting gap above T(c) is one of the central questions in high-T(c) research. Although some experimental evidence suggests that the two gaps are distinct, this issue is still under intense debate. A crucial piece of evidence to firmly establish this two-gap picture is still missing: a direct and unambiguous observation of a single-particle gap tied to the superconducting transition as function of temperature. Here we report the discovery of such an energy gap in underdoped Bi2Sr2CaCu2O8+delta in the momentum space region overlooked in previous measurements. Near the diagonal of Cu-O bond direction (nodal direction), we found a gap that opens at T(c) and has a canonical (BCS-like) temperature dependence accompanied by the appearance of the so-called Bogoliubov quasi-particles, a classical signature of superconductivity. This is in sharp contrast to the pseudogap near the Cu-O bond direction (antinodal region) measured in earlier experiments.     

Ecology: diversity and stability in plant communities

The relationship between species diversity and ecosystem stability is controversial. Tilman et al. analyse biomass patterns over a decade in a grassland experiment with artificial plant communities, and provide evidence for a positive relationship between the number of plant species and the temporal stability of the ecosystem. Here we use data from a long-term biodiversity experiment with plant communities that were not controlled by weeding in order to show that diverse systems can be both stable and unstable.     

A dynamic early East Antarctic Ice Sheet suggested by ice-covered fjord landscapes

The first Cenozoic ice sheets initiated in Antarctica from the Gamburtsev Subglacial Mountains and other highlands as a result of rapid global cooling ～34 million years ago. In the subsequent 20 million years, at a time of declining atmospheric carbon dioxide concentrations and an evolving Antarctic circumpolar current, sedimentary sequence interpretation and numerical modelling suggest that cyclical periods of ice-sheet expansion to the continental margin, followed by retreat to the subglacial highlands, occurred up to thirty times. These fluctuations were paced by orbital changes and were a major influence on global sea levels. Ice-sheet models show that the nature of such oscillations is critically dependent on the pattern and extent of Antarctic topographic lowlands. Here we show that the basal topography of the Aurora Subglacial Basin of East Antarctica, at present overlain by 2-4.5?km of ice, is characterized by a series of well-defined topographic channels within a mountain block landscape. The identification of this fjord landscape, based on new data from ice-penetrating radar, provides an improved understanding of the topography of the Aurora Subglacial Basin and its surroundings, and reveals a complex surface sculpted by a succession of ice-sheet configurations substantially different from today's. At different stages during its fluctuations, the edge of the East Antarctic Ice Sheet lay pinned along the margins of the Aurora Subglacial Basin, the upland boundaries of which are currently above sea level and the deepest parts of which are more than 1?km below sea level. Although the timing of the channel incision remains uncertain, our results suggest that the fjord landscape was carved by at least two iceflow regimes of different scales and directions, each of which would have over-deepened existing topographic depressions, reversing valley floor slopes.     

Ebola virus entry requires the cholesterol transporter Niemann-Pick C1

Infections by the Ebola and Marburg filoviruses cause a rapidly fatal haemorrhagic fever in humans for which no approved antivirals are available. Filovirus entry is mediated by the viral spike glycoprotein (GP), which attaches viral particles to the cell surface, delivers them to endosomes and catalyses fusion between viral and endosomal membranes. Additional host factors in the endosomal compartment are probably required for viral membrane fusion; however, despite considerable efforts, these critical host factors have defied molecular identification. Here we describe a genome-wide haploid genetic screen in human cells to identify host factors required for Ebola virus entry. Our screen uncovered 67 mutations disrupting all six members of the homotypic fusion and vacuole protein-sorting (HOPS) multisubunit tethering complex, which is involved in the fusion of endosomes to lysosomes, and 39 independent mutations that disrupt the endo/lysosomal cholesterol transporter protein Niemann-Pick C1 (NPC1). Cells defective for the HOPS complex or NPC1 function, including primary fibroblasts derived from human Niemann-Pick type C1 disease patients, are resistant to infection by Ebola virus and Marburg virus, but remain fully susceptible to a suite of unrelated viruses. We show that membrane fusion mediated by filovirus glycoproteins and viral escape from the vesicular compartment require the NPC1 protein, independent of its known function in cholesterol transport. Our findings uncover unique features of the entry pathway used by filoviruses and indicate potential antiviral strategies to combat these deadly agents.