Branched integumental structures in Sinornithosaurus and the origin of feathers

The evolutionary origin of feathers has long been obscured because no morphological antecedents were known to the earliest, structurally modern feathers of Archaeopteryx. It has been proposed that the filamentous integumental appendages on several theropod dinosaurs are primitive feathers; but the homology between these filamentous structures and feathers has been disputed, and two taxa with true feathers (Caudipteryx and Protarchaeopteryx) have been proposed to be flightless birds. Confirmation of the theropod origin of feathers requires documentation of unambiguously feather-like structures in a clearly non-avian theropod. Here we describe our observations of the filamentous integumental appendages of the basal dromaeosaurid dinosaur Sinornithosaurus millenii, which indicate that they are compound structures composed of multiple filaments. Furthermore, these appendages exhibit two types of branching structure that are unique to avian feathers: filaments joined in a basal tuft, and filaments joined at their bases in series along a central filament. Combined with the independent phylogenetic evidence supporting the theropod ancestry of birds, these observations strongly corroborate the hypothesis that the integumental appendages of Sinornithosaurus are homologous with avian feathers. The plesiomorphic feathers of Sinornithosaurus also conform to the predictions of an independent, developmental model of the evolutionary origin of feathers.     

Mutations in the gene encoding lecithin retinol acyltransferase are associated with early-onset severe retinal dystrophy

The chromophore of the visual pigments, 11-cis retinal, is derived from vitamin A (all-trans retinol) through a series of reactions that take place in retinal pigment epithelium (RPE); (ref. 1). The first of these reactions is catalyzed by lecithin retinol acyltransferase (LRAT); (ref. 2). We screened 267 retinal dystrophy patients for mutations in LRAT and identified disease-associated mutations (S175R and 396delAA) in three individuals with severe, early-onset disease. We showed that the S175R mutant has no acyltransferase activity in transfected COS-7 cells. Our findings highlight the importance of genetic defects in vitamin A metabolism as causes of retinal dystrophies and extend prospects for retinoid replacement therapy in this group of diseases.     

Dominant effector genetics in mammalian cells

We have expressed libraries of peptides in mammalian cells to select for trans-dominant effects on intracellular signaling systems. As an example-and to reveal pharmacologically relevant points in pathways that lead to Taxol resistance-we selected for peptide motifs that confer resistance to Taxol-induced cell death. Of several peptides selected, one, termed RGP8.5, was linked to upregulation of expression of the gene ABCB1 (also known as MDR1, for multiple drug resistance) in HeLa cells. Our data indicate that trans-dominant effector peptides can point to potential mechanisms by which signaling systems operate. Such tools may be useful in functional genomic analysis of signaling pathways in mammalian disease processes.     

Earliest presence of humans in northeast Asia

The timing of the earliest habitation and oldest stone technologies in different regions of the world remains a contentious topic in the study of human evolution. Here we contribute to this debate with detailed magnetostratigraphic results on two exposed parallel sections of lacustrine sediments at Xiaochangliang in the Nihewan Basin, north China; these results place stringent controls on the age of Palaeolithic stone artifacts that were originally reported over two decades ago. Our palaeomagnetic findings indicate that the artifact layer resides in a reverse polarity magnetozone bounded by the Olduvai and Jaramillo subchrons. Coupled with an estimated rate of sedimentation, these findings constrain the layer's age to roughly 1.36 million years ago. This result represents the age of the oldest known stone assemblage comprising recognizable types of Palaeolithic tool in east Asia, and the earliest definite occupation in this region as far north as 40 degrees N.     

Shor整数分解量子算法的加速实现

基于半经典量子Fourier变换的实现方法,提出了整数k的3元二进制表示生成向量和生成函数概念,构造了生成函数的真值表,证明了由其逐比特生成的整数k的3元二进制表示向量是整数k的一种NAF表示,且表示中非0元个数的最大值为[(「logk■+1)2],并基于此重新设计了Shor算法的量子实现线路.与Parker的Shor算法量子实现线路相比,计算资源大体相同(所需的基本量子门数量均为O(「logN■3),所需的量子比特数量前者较后者多2量子比特),但实现速度提高了2倍.     

Multisite phosphorylation of a CDK inhibitor sets a threshold for the onset of DNA replication.

SCF ubiquitin ligases target phosphorylated substrates for ubiquitin-dependent proteolysis by means of adapter subunits called F-box proteins. The F-box protein Cdc4 captures phosphorylated forms of the cyclin-dependent kinase inhibitor Sic1 for ubiquitination in late G1 phase, an event necessary for the onset of DNA replication. The WD40 repeat domain of Cdc4 binds with high affinity to a consensus phosphopeptide motif (the Cdc4 phospho-degron, CPD), yet Sic1 itself has many sub-optimal CPD motifs that act in concert to mediate Cdc4 binding. The weak CPD sites in Sic1 establish a phosphorylation threshold that delays degradation in vivo, and thereby establishes a minimal G1 phase period needed to ensure proper DNA replication. Multisite phosphorylation may be a more general mechanism to set thresholds in regulated protein-protein interactions.     

ATR/ATM-mediated phosphorylation of human Rad17 is required for genotoxic stress responses.

Genotoxic stress triggers the activation of checkpoints that delay cell-cycle progression to allow for DNA repair. Studies in fission yeast implicate members of the Rad family of checkpoint proteins, which includes Rad17, Rad1, Rad9 and Hus1, as key early-response elements during the activation of both the DNA damage and replication checkpoints. Here we demonstrate a direct regulatory linkage between the human Rad17 homologue (hRad17) and the checkpoint kinases, ATM and ATR. Treatment of human cells with genotoxic agents induced ATM/ATR-dependent phosphorylation of hRad17 at Ser 635 and Ser 645. Overexpression of a hRad17 mutant (hRad17AA) bearing Ala substitutions at both phosphorylation sites abrogated the DNA-damage-induced G2 checkpoint, and sensitized human fibroblasts to genotoxic stress. In contrast to wild-type hRad17, the hRad17AA mutant showed no ionizing-radiation-inducible association with hRad1, a component of the hRad1-hRad9-hHus1 checkpoint complex. These findings demonstrate that ATR/ATM-dependent phosphorylation of hRad17 is a critical early event during checkpoint signalling in DNA-damaged cells.     

Effects of Ru on microstructure stability and mechanical properties of Ni3Al single crystal alloy

The effect of Ru on microstructure stability and stress rupture properties of a Ni3Al single-crystal alloy was investigated. The experimental results showed that the addition of 2% Ru (mass fraction) improved the microstructure stability due to the res traint of harmful Y-NiMo phase formation during the thermal exposure at the high temperature above 1 000 °C. And the reason may be that the addition of Ru increased the degree of Mo supersaturation in both γ and γ′ phases, and hence suppressed the precipitation of Y-NiMo phase. The results of stress rupture tests under the testing condition of 1 100 °C, 120 MPa showed that the addition of 2% Ru in the alloy improved the stress rupture lives significantly for ther mal exposed samples. The improvement of the stress rupture properties may be attributed to the restraint of Y-NiMo phase precipitation and growth by the addition of the proper amount Ru.