西北太平洋浮游有孔虫的SSU rDNA序列及其古海洋学意义

研究对采集于西北太平洋冲绳海槽表层水体中的活浮游有孔虫进行DNA分析尝试，获得了西北太平洋浮游有孔虫Pulleniatina obliquiloculata 和Globigerina sp.等的SSU rDNA序列特征，并与南太平洋地区属种的DNA序列进行对比. 结果显示两不同海区P.obliquiloculata个体的SSU rDNA差异与同一个体内不同拷贝序列间差异类似，仅为0.7%—1.2%. 详细比较研究认为，传统微体古生物形态学定义种对西北太平洋与南太平洋的P.obliquiloculata来说具有可靠的分子生物学证据.     

Do professional forecasters believe in the Phillips curve? evidence from the G7 countries

This paper uses monthly survey data for the G7 countries for the time period 1989–2007 to explore the link between expectations on nominal wages, prices and unemployment rates as suggested by the wage and price Phillips curves. Four major findings stand out. First, we find that survey participants trust in both types of Phillips curve relationships. Second, we find evidence in favor of nonlinearities in the price Phillips curve. Third, we take into account a kink in the price Phillips curve to indicate that the slope of the Phillips curve differs during the business cycle. We find strong evidence of this feature in the data which confirms recent theoretical discussions. Fourth, we employ our data to the expectations‐augmented Phillips curve model. The results suggest that professional forecasters adopt this model when forecasting macroeconomic variables. Copyright © 2010 John Wiley & Sons, Ltd.     

The bipolar mitotic kinesin Eg5 moves on both microtubules that it crosslinks

During cell division, mitotic spindles are assembled by microtubule-based motor proteins. The bipolar organization of spindles is essential for proper segregation of chromosomes, and requires plus-end-directed homotetrameric motor proteins of the widely conserved kinesin-5 (BimC) family. Hypotheses for bipolar spindle formation include the 'push-pull mitotic muscle' model, in which kinesin-5 and opposing motor proteins act between overlapping microtubules. However, the precise roles of kinesin-5 during this process are unknown. Here we show that the vertebrate kinesin-5 Eg5 drives the sliding of microtubules depending on their relative orientation. We found in controlled in vitro assays that Eg5 has the remarkable capability of simultaneously moving at approximately 20 nm s(-1) towards the plus-ends of each of the two microtubules it crosslinks. For anti-parallel microtubules, this results in relative sliding at approximately 40 nm s(-1), comparable to spindle pole separation rates in vivo. Furthermore, we found that Eg5 can tether microtubule plus-ends, suggesting an additional microtubule-binding mode for Eg5. Our results demonstrate how members of the kinesin-5 family are likely to function in mitosis, pushing apart interpolar microtubules as well as recruiting microtubules into bundles that are subsequently polarized by relative sliding.     

Trans-SNARE pairing can precede a hemifusion intermediate in intracellular membrane fusion

The question concerning whether all membranes fuse according to the same mechanism has yet to be answered satisfactorily. During fusion of model membranes or viruses, membranes dock, the outer membrane leaflets mix (termed hemifusion), and finally the fusion pore opens and the contents mix. Viral fusion proteins consist of a membrane-disturbing 'fusion peptide' and a helical bundle that pin the membranes together. Although SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) complexes form helical bundles with similar topology, it is unknown whether SNARE-dependent fusion events on intracellular membranes proceed through a hemifusion state. Here we identify the first hemifusion state for SNARE-dependent fusion of native membranes, and place it into a sequence of molecular events: formation of helical bundles by SNAREs precedes hemifusion; further progression to pore opening requires additional peptides. Thus, SNARE-dependent fusion may proceed along the same pathway as viral fusion: both use a docking mechanism via helical bundles and additional peptides to destabilize the membrane and efficiently induce lipid mixing. Our results suggest that a common lipidic intermediate may underlie all fusion reactions of lipid bilayers.     

A new family of RhoGEFs activates the Rop molecular switch in plants

In plants, the small GTP-binding proteins called Rops work as signalling switches that control growth, development and plant responses to various environmental stimuli. Rop proteins (Rho of plants, Rac-like and AtRac in Arabidopsis thaliana) belong to the Rho family of Ras-related GTP-binding proteins that turn on signalling pathways by switching from a GDP-bound inactive to a GTP-bound active conformation. Activation depends on guanine nucleotide exchange factors (GEFs) that catalyse the otherwise slow GDP dissociation for subsequent GTP binding. Although numerous RhoGEFs exist in animals and yeasts, no Rop-specific GEFs have yet been identified in plants and so Rop activation has remained elusive. Here we describe a new family of RhoGEF proteins that are exclusive to plants. We define a unique domain within these RopGEFs, termed PRONE (plant-specific Rop nucleotide exchanger), which is exclusively active towards members of the Rop subfamily. It increases nucleotide dissociation from Rop more than a thousand-fold and forms a tight complex with nucleotide-free Rop. RopGEFs may represent the missing link in signal transduction from receptor kinases to Rops and their identification has implications for the evolution of the Rho molecular switch.     

Parity-time synthetic photonic lattices

The development of new artificial structures and materials is today one of the major research challenges in optics. In most studies so far, the design of such structures has been based on the judicious manipulation of their refractive index properties. Recently, the prospect of simultaneously using gain and loss was suggested as a new way of achieving optical behaviour that is at present unattainable with standard arrangements. What facilitated these quests is the recently developed notion of 'parity-time symmetry' in optical systems, which allows a controlled interplay between gain and loss. Here we report the experimental observation of light transport in large-scale temporal lattices that are parity-time symmetric. In addition, we demonstrate that periodic structures respecting this symmetry can act as unidirectional invisible media when operated near their exceptional points. Our experimental results represent a step in the application of concepts from parity-time symmetry to a new generation of multifunctional optical devices and networks.     

Driver mutations in histone H3.3 and chromatin remodelling genes in paediatric glioblastoma

Glioblastoma multiforme (GBM) is a lethal brain tumour in adults and children. However, DNA copy number and gene expression signatures indicate differences between adult and paediatric cases. To explore the genetic events underlying this distinction, we sequenced the exomes of 48 paediatric GBM samples. Somatic mutations in the H3.3-ATRX-DAXX chromatin remodelling pathway were identified in 44% of tumours (21/48). Recurrent mutations in H3F3A, which encodes the replication-independent histone 3 variant H3.3, were observed in 31% of tumours, and led to amino acid substitutions at two critical positions within the histone tail (K27M, G34R/G34V) involved in key regulatory post-translational modifications. Mutations in ATRX (α-thalassaemia/mental retardation syndrome X-linked) and DAXX (death-domain associated protein), encoding two subunits of a chromatin remodelling complex required for H3.3 incorporation at pericentric heterochromatin and telomeres, were identified in 31% of samples overall, and in 100% of tumours harbouring a G34R or G34V H3.3 mutation. Somatic TP53 mutations were identified in 54% of all cases, and in 86% of samples with H3F3A and/or ATRX mutations. Screening of a large cohort of gliomas of various grades and histologies (n = 784) showed H3F3A mutations to be specific to GBM and highly prevalent in children and young adults. Furthermore, the presence of H3F3A/ATRX-DAXX/TP53 mutations was strongly associated with alternative lengthening of telomeres and specific gene expression profiles. This is, to our knowledge, the first report to highlight recurrent mutations in a regulatory histone in humans, and our data suggest that defects of the chromatin architecture underlie paediatric and young adult GBM pathogenesis.