Regulation of cellulose synthesis in Acetobacter xylinum by cyclic diguanylic acid

Cellulose is the most abundant renewable carbon resource on earth and is an indispensable raw material for the wood, paper, and textile industries. A model system to study the mechanism of cellulose biogenesis is the bacterium Acetobacter xylinum which produces pure cellulose as an extracellular product. It was from this organism that in vitro preparations which possessed high levels of cellulose synthase activity were first obtained in both membranous and soluble forms. We recently demonstrated that this activity is subject to a complex multi-component regulatory system, in which the synthase is directly affected by an unusual cyclic nucleotide activator enzymatically formed from GTP, and indirectly by a Ca (2+) -sensitive phosphodiesterase which degrades the activator. The cellulose synthase activator (CSA) has now been identified as bis-(3' 5')-cyclic diguanylic acid (5'G3'p5'G3'p) on the basis of mass spectroscopic data, nuclear magnetic resonance analysis and comparison with chemically synthesized material. We also report here on intermediary steps in the synthesis and degradation of this novel circular dinucleotide, which have been integrated into a model for the regulation of cellulose synthesis.     

Acetylation-dependent regulation of endothelial Notch signalling by the SIRT1 deacetylase

Notch signalling is a key intercellular communication mechanism that is essential for cell specification and tissue patterning, and which coordinates critical steps of blood vessel growth. Although subtle alterations in Notch activity suffice to elicit profound differences in endothelial behaviour and blood vessel formation, little is known about the regulation and adaptation of endothelial Notch responses. Here we report that the NAD(+)-dependent deacetylase SIRT1 acts as an intrinsic negative modulator of Notch signalling in endothelial cells. We show that acetylation of the Notch1 intracellular domain (NICD) on conserved lysines controls the amplitude and duration of Notch responses by altering NICD protein turnover. SIRT1 associates with NICD and functions as a NICD deacetylase, which opposes the acetylation-induced NICD stabilization. Consequently, endothelial cells lacking SIRT1 activity are sensitized to Notch signalling, resulting in impaired growth, sprout elongation and enhanced Notch target gene expression in response to DLL4 stimulation, thereby promoting a non-sprouting, stalk-cell-like phenotype. In vivo, inactivation of Sirt1 in zebrafish and mice causes reduced vascular branching and density as a consequence of enhanced Notch signalling. Our findings identify reversible acetylation of the NICD as a molecular mechanism to adapt the dynamics of Notch signalling, and indicate that SIRT1 acts as rheostat to fine-tune endothelial Notch responses.     

中小企业技术创新的现状与对策

分析了中国中小企业技术创新的特点和现状,指出中小企业技术创新能力不高、缺乏技术创新的人才队伍、产学研合作机制不健全、融资渠道少等问题,提出重视中小企业技术创新人才的培养、优化金融环境、建立健全产学研合作机制、通过培育中介组织推动企业自主创新、选择适合企业实际情况的技术创新战略等措施.     

人体经络复杂网络路由问题的求解

为了研究经络—免疫—神经—内分泌网络(jingluo-immune-nerve-endocrinenetwork)学说,采用复杂网络定义、模型、算法和理论,对穴位在经络中的信息传递方式、交互条件、路由途径、高导电性进行了测试和验证,建立了经络的复杂网络路由模型,证实了该网络的存在·信息物质沿经络路线传播,经络循行也有确定的方向和速度,确立了经络的基本功能是传递及调控生命信息物质为经络研究开辟了一条新的方法·     

互联网中的标准结构熵的时间演化分析

通过对Internet标准结构熵随时间变化规律的分析发现,Internet的标准结构熵具有随时间而逐渐降低的趋势,以riesling节点获得的Internet监测数据的计算结果为例,Internet标准结构熵从2000年4月的最大值0.379下降至2004年5月的0.318,月平均下降幅度为0.12%,即由高熵值拓扑结构向低熵值拓扑结构的状态变化.由此可知Internet的宏观拓扑结构在演化过程中存在着拓扑结构的信息代谢.     

基于VC和VIP的面向对象知识表示

知识表示是人工智能研究的基本问题之一。通过在 Visual C+ +的类中引入Visual Prolog的推理机制提出了一种基于 VC和 VIP的面向对象知识表示方法 ,完善了 Visual C+ +对象的推理功能 ,进一步增强了面向对象的知识表示能力以及 VisualProlog的接口和计算能力 ,并通过实验验证了方法的性能     

The genome sequence of the filamentous fungus Neurospora crassa

Neurospora crassa is a central organism in the history of twentieth-century genetics, biochemistry and molecular biology. Here, we report a high-quality draft sequence of the N. crassa genome. The approximately 40-megabase genome encodes about 10,000 protein-coding genes--more than twice as many as in the fission yeast Schizosaccharomyces pombe and only about 25% fewer than in the fruitfly Drosophila melanogaster. Analysis of the gene set yields insights into unexpected aspects of Neurospora biology including the identification of genes potentially associated with red light photobiology, genes implicated in secondary metabolism, and important differences in Ca2+ signalling as compared with plants and animals. Neurospora possesses the widest array of genome defence mechanisms known for any eukaryotic organism, including a process unique to fungi called repeat-induced point mutation (RIP). Genome analysis suggests that RIP has had a profound impact on genome evolution, greatly slowing the creation of new genes through genomic duplication and resulting in a genome with an unusually low proportion of closely related genes.     

Disruption of Cnp1 uncouples oligodendroglial functions in axonal support and myelination

Myelination of axons by oligodendrocytes enables rapid impulse propagation in the central nervous system. But long-term interactions between axons and their myelin sheaths are poorly understood. Here we show that Cnp1, which encodes 2',3'-cyclic nucleotide phosphodiesterase in oligodendrocytes, is essential for axonal survival but not for myelin assembly. In the absence of glial cyclic nucleotide phosphodiesterase, mice developed axonal swellings and neurodegeneration throughout the brain, leading to hydrocephalus and premature death. But, in contrast to previously studied myelin mutants, the ultrastructure, periodicity and physical stability of myelin were not altered in these mice. Genetically, the chief function of glia in supporting axonal integrity can thus be completely uncoupled from its function in maintaining compact myelin. Oligodendrocyte dysfunction, such as that in multiple sclerosis lesions, may suffice to cause secondary axonal loss.