活性氧与植物防卫反应

目的：总结分析活性氧在植物防卫反应中的作用。方法：根据近10年内公开发表的20篇中英文文献对活性氧的种类、特性，以及在植物抗病过程中所起的作用进行较全面的总结。结果：介绍活性氧的种类、性质，着重讨论了活性氧的产生和消除机理；并对当前该领域今后的研究方向进行了展望。结论：活性氧在植物防卫反应过程中起双重作用，即高浓度时对植物起伤害作用，低浓度时起信号传递作用诱导植物抗性基因和防卫基因的表达。     

盐胁迫对两种忍冬属植物活性氧平衡的影响

以红白忍冬和郁香忍冬盆栽苗为试验材料,研究不同浓度的NaCl胁迫对两者生理指标的影响,并比较它们的耐盐性差异。结果表明,在盐胁迫条件下,两种植物叶片的电导率、MDA含量均不断上升。胁迫期间,红白忍冬的H2O2含量相对于对照没有明显变化,O.2-产生速率在处理前期明显上升,上升出现的时间迟于郁香忍冬;而郁香忍冬的H2O2含量一直维持较高水平,O.2-产生速率在处理前期也有所增加。红白忍冬的SOD、APX和CAT活性总体表现出先上升后下降的趋势,而POD活性则一直上升。郁香忍冬在胁迫期间,其SOD活性有小幅增加;APX和CAT的活性均呈现先上升后下降的趋势;POD活性前期没有明显增加,在处理终期时也仅在100mmol/L胁迫下才显著增加。表明两种植物在遭受盐胁迫时,均能启动抗氧化酶系统来清除活性氧,降低氧化胁迫的伤害。同时,相对于郁香忍冬,红白忍冬通过快速上调抗氧化酶活性,降低盐胁迫对膜脂过氧化作用,保持膜的完整性,从而更好地抵御氧化损害更耐受盐胁迫。     

Reactive oxygen species produced by NADPH oxidase regulate plant cell growth

Cell expansion is a central process in plant morphogenesis, and the elongation of roots and root hairs is essential for uptake of minerals and water from the soil. Ca2+ influx from the extracellular store is required for (and sets the rates of) cell elongation in roots. Arabidopsis thaliana rhd2 mutants are defective in Ca2+ uptake and consequently cell expansion is compromised--rhd2 mutants have short root hairs and stunted roots. To determine the regulation of Ca2+ acquisition in growing root cells we show here that RHD2 is an NADPH oxidase, a protein that transfers electrons from NADPH to an electron acceptor leading to the formation of reactive oxygen species (ROS). We show that ROS accumulate in growing wild-type (WT) root hairs but their levels are markedly decreased in rhd2 mutants. Blocking the activity of the NADPH oxidase with diphenylene iodonium (DPI) inhibits ROS formation and phenocopies Rhd2-. Treatment of rhd2 roots with ROS partly suppresses the mutant phenotype and stimulates the activity of plasma membrane hyperpolarization-activated Ca2+ channels, the predominant root Ca2+ acquisition system. This indicates that NADPH oxidases control development by making ROS that regulate plant cell expansion through the activation of Ca2+ channels.     

A central role for JNK in obesity and insulin resistance

Obesity is closely associated with insulin resistance and establishes the leading risk factor for type 2 diabetes mellitus, yet the molecular mechanisms of this association are poorly understood. The c-Jun amino-terminal kinases (JNKs) can interfere with insulin action in cultured cells and are activated by inflammatory cytokines and free fatty acids, molecules that have been implicated in the development of type 2 diabetes. Here we show that JNK activity is abnormally elevated in obesity. Furthermore, an absence of JNK1 results in decreased adiposity, significantly improved insulin sensitivity and enhanced insulin receptor signalling capacity in two different models of mouse obesity. Thus, JNK is a crucial mediator of obesity and insulin resistance and a potential target for therapeutics.     

活性氧与植物抗病性的关系

病原菌侵入植物后可诱导活性氧的出发，并且在非寄主互作中比寄 互作中活性氧的积累更明显。我们在禾谷类作物与白粉菌互作的研究中，也得到了同样的结论。活性氧迸发已被认为是寄主防卫反应之一，在植物的抗病性中具有很重要的作用。     

2型糖尿病胰岛素抵抗研究进展

胰岛素抵抗和B细胞功能障碍是2型糖尿病发病机制的两个主要环节,而胰岛素抵抗是2型糖尿病发生的始动因素.研究发现,信号蛋白异常和炎症因子与胰岛素抵抗的发生密切相关,探讨其相关关系为治疗糖尿病、防治或延缓其并发症的发生提供重要的科学依据.     

Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis

Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis.     

基于AP算法的多物种同源功能模块挖掘算法

提出了一种多物种代谢网络同源功能模块的挖掘算法.依据物种间的亲缘关系,给出一种新的化合物相似度定义方式,使用AP算法进行模块的初始划分,然后按照模块的同源系数逐层进行重叠扩展.使用65种不同生物的代谢网络进行实验研究,结果表明：得到的保守功能模块与KEGG数据库提供的参考功能模块具有较高匹配率,外围功能模块体现了功能模块在不同物种内的分布差异,验证了算法的有效性.     

Slow inward calcium currents have no obvious role in muscle excitation-contraction coupling

It has been proposed that an influx of calcium ions into twitch muscle fibres during an action potential might initiate contraction. However, when external Ca2+ is lowered to 10(-8) M with EGTA, the fibres can produce normal twitches for many minutes. Nevertheless, a clear Ca2+ influx during contraction has been demonstrated, and it has been found that phasic skeletal muscle has an inward calcium current (ICa) which can give rise to calcium spikes. In certain conditions, a reduction in external Ca2+ with 80-90 mM EGTA results in reversible blockade of excitation-contraction (e-c) coupling, leading some authors to suggest that extracellular Ca2+ moved into the myoplasm due to ICa may be involved in the e-c coupling mechanism that triggers contraction. This proposition was further supported by the localization of ICa in the T-system, which circumvented the problem of the delay due to calcium diffusion from the surface membrane. We have now investigated whether ICa has a clear role in initiating or sustaining contractions in twitch muscle fibres. Our approach was to decrease or eliminate ICa with the calcium-blocking agent diltiazem (Herbesser) and to see how the twitch, tetanic and potassium-contracture tensions were affected. We found that ICa could be decreased or cancelled with the calcium-blocking agent, but that the same concentration of the drug potentiated the twitch, tetanus and contractures. We conclude, therefore, that ICa has no role in e-c coupling. A preliminary report of these results has been presented elsewhere.     

Genetic evidence that FGFs have an instructive role in limb proximal-distal patterning

Half a century ago, the apical ectodermal ridge (AER) at the distal tip of the tetrapod limb bud was shown to produce signals necessary for development along the proximal-distal (P-D) axis, but how these signals influence limb patterning is still much debated. Fibroblast growth factor (FGF) gene family members are key AER-derived signals, with Fgf4, Fgf8, Fgf9 and Fgf17 expressed specifically in the mouse AER. Here we demonstrate that mouse limbs lacking Fgf4, Fgf9 and Fgf17 have normal skeletal pattern, indicating that Fgf8 is sufficient among AER-FGFs to sustain normal limb formation. Inactivation of Fgf8 alone causes a mild skeletal phenotype; however, when we also removed different combinations of the other AER-FGF genes, we obtained unexpected skeletal phenotypes of increasing severity, reflecting the contribution that each FGF can make to the total AER-FGF signal. Analysis of the compound mutant limb buds revealed that, in addition to sustaining cell survival, AER-FGFs regulate P-D-patterning gene expression during early limb bud development, providing genetic evidence that AER-FGFs function to specify a distal domain and challenging the long-standing hypothesis that AER-FGF signalling is permissive rather than instructive for limb patterning. We discuss how a two-signal model for P-D patterning can be integrated with the concept of early specification to explain the genetic data presented here.     

DNA cloning in Streptomyces: resistance genes from antibiotic-producing species

The biochemical and morphological differentiation of actinomycetes makes them academically and economically interesting. Their secondary metabolites provide the majority of medically and agriculturally important antibiotics (streptomycete genes may also be the primary source of clinically important antibiotic resistance); their complex morphological developmental cycle involves a series of changes from vegetative mycelial growth to spore formation. Recombinant DNA technology would add a powerful new dimension to the analysis of these various aspects of actinomycete biology and would also facilitate the development of industrial strains with increased antibiotic yield, or capable of making new antibiotics. For most of these purposes, cloning of genes within and between actinomycetes is required to study the expression of particular genes in genetic backgrounds defined by mutations of the characters under study. To achieve this, we have now developed a method for molecular cloning involving the transfer of genes between unrelated streptomycetes.