Structure of the nucleosome core particle at 7 A resolution

The crystal structure of the nucleosome core particle has been solved to 7 A resolution. The right-handed B-DNA superhelix on the outside contains several sharp bends and makes numerous interactions with the histone octamer within. The central turn of superhelix and H3 . H4 tetramer have dyad symmetry, but the H2A . H2B dimers show departures due to interparticle associations.     

The structure of DNA in the nucleosome core

The 1.9-A-resolution crystal structure of the nucleosome core particle containing 147 DNA base pairs reveals the conformation of nucleosomal DNA with unprecedented accuracy. The DNA structure is remarkably different from that in oligonucleotides and non-histone protein-DNA complexes. The DNA base-pair-step geometry has, overall, twice the curvature necessary to accommodate the DNA superhelical path in the nucleosome. DNA segments bent into the minor groove are either kinked or alternately shifted. The unusual DNA conformational parameters induced by the binding of histone protein have implications for sequence-dependent protein recognition and nucleosome positioning and mobility. Comparison of the 147-base-pair structure with two 146-base-pair structures reveals alterations in DNA twist that are evidently common in bulk chromatin, and which are of probable importance for chromatin fibre formation and chromatin remodelling.     

卤素离子在多晶铜电极表面的微分电容研究

本文通过测量金属晶体电极表面的微分电容研究了金属电极表面在金属与水溶液界面上的吸附能力,以及金属与吸附质之间的相互作用。文中论述了多晶铜电极在(0.5-x)mNaClO_4+xmNaBr的一系列不同x值的溶液中的微分电容测量值及微分电容-电位曲线,证明了F~-和ClO_4~-离子在多晶铜电极表面是非常弱的吸附,Br~-离子在多晶铜电极表面具有特定的吸附,每条电容-电位曲线有一个凸起的峰。在峰所对应的位能值,金属表面对阴离子的吸附能力强,证实金属-吸附质之间的相互作用强,吸附的阴离子在过渡层中散射导电电子的能力也强。对于相同阴离子和金属的体系,其微分电容与吸附质的浓度、电压、溶液的pH值和表面的非均匀性等因素密切有关。研究证明,金属晶体电极表面在电解质溶液中的微分电容的变化规律类似于表面电反射信号的强弱变化规律,微分电容大小取决于金属-吸附质之间的电荷转移程度。     

SNF-6 is an acetylcholine transporter interacting with the dystrophin complex in Caenorhabditis elegans

Muscular dystrophies are among the most common human genetic diseases and are characterized by progressive muscle degeneration. Muscular dystrophies result from genetic defects in components of the dystrophin-glycoprotein complex (DGC), a multimeric complex found in the muscle cell plasma membrane. The DGC links the intracellular cytoskeleton to the extracellular matrix and is thought to be important for maintaining the mechanical integrity of muscles and organizing signalling molecules. The exact role of the DGC in the pathogenesis of disease has, however, remained uncertain. Mutations in Caenorhabditis elegans DGC genes lead to specific defects in coordinated movement and can also cause muscle degeneration. Here we show that mutations in the gene snf-6 result in phenotypes indistinguishable from those of the DGC mutants, and that snf-6 encodes a novel acetylcholine/choline transporter. SNF-6 mediates the uptake of acetylcholine at neuromuscular junctions during periods of increased synaptic activity. SNF-6 also interacts with the DGC, and mutations in DGC genes cause a loss of SNF-6 at neuromuscular junctions. Improper clearing of acetylcholine and prolonged excitation of muscles might contribute to the pathogenesis of muscular dystrophies.     

平板式光生物反应器的Parietochloris incisa超高密度培养

利用平板式光生物反应器对一种新分离的微藻Parietochlorisincisa进行了室外放大培养研究。在最适培养条件下 ,实现了对该微藻的超高密度培养 ,使单位培养体积和单位培养面积的细胞生物量分别达到了 7.35g/ (L·d)和 96 .12 g/ (m2 ·d)     

Structure and mechanism of the chromatin remodelling factor ISW1a

Site-specific recognition of DNA in eukaryotic organisms depends on the arrangement of nucleosomes in chromatin. In the yeast Saccharomyces cerevisiae, ISW1a and related chromatin remodelling factors are implicated in establishing the nucleosome repeat during replication and altering nucleosome position to affect gene activity. Here we have solved the crystal structures of S. cerevisiae ISW1a lacking its ATPase domain both alone and with DNA bound at resolutions of 3.25?? and 3.60??, respectively, and we have visualized two different nucleosome-containing remodelling complexes using cryo-electron microscopy. The composite X-ray and electron microscopy structures combined with site-directed photocrosslinking analyses of these complexes suggest that ISW1a uses a dinucleosome substrate for chromatin remodelling. Results from a remodelling assay corroborate the dinucleosome model. We show how a chromatin remodelling factor could set the spacing between two adjacent nucleosomes acting as a 'protein ruler'.     

An open form of syntaxin bypasses the requirement for UNC-13 in vesicle priming.

The priming step of synaptic vesicle exocytosis is thought to require the formation of the SNARE complex, which comprises the proteins synaptobrevin, SNAP-25 and syntaxin. In solution syntaxin adopts a default, closed configuration that is incompatible with formation of the SNARE complex. Specifically, the amino terminus of syntaxin binds the SNARE motif and occludes interactions with the other SNARE proteins. The N terminus of syntaxin also binds the presynaptic protein UNC-13 (ref. 5). Studies in mouse, Drosophila and Caenorhabditis elegans suggest that UNC-13 functions at a post-docking step of exocytosis, most likely during synaptic vesicle priming. Therefore, UNC-13 binding to the N terminus of syntaxin may promote the open configuration of syntaxin. To test this model, we engineered mutations into C. elegans syntaxin that cause the protein to adopt the open configuration constitutively. Here we demonstrate that the open form of syntaxin can bypass the requirement for UNC-13 in synaptic vesicle priming. Thus, it is likely that UNC-13 primes synaptic vesicles for fusion by promoting the open configuration of syntaxin.