植物天然免疫系统研究进展

很多植物病原菌严重地损害植物的生长和繁殖。植物与病原体协同进化过程中,也逐渐形成了一系列复杂高效的保护机制来抵御病原物的侵染。植物中抵抗外界微生物刺激所形成的系统被称为植物天然免疫系统,可分为两个层次。第1个层次是植物模式识别受体(PRRs)识别病原相关分子模式(PAMPs),触发病原相关分子模式触发的免疫反应（PTI）,激活植物体中促丝裂原活化蛋白激酶(MAPK)信号通路使植物产生早期应答反应。PTI适应性较广,可识别和响应包括非致病菌的许多类微生物。第2个层次是病原菌产生效应因子抑制基础免疫响应PTI,而植物产生针对性更强的抗性蛋白(R蛋白)识别效应因子,并通过效应因子触发型免疫(ETI)来重建植物的抗性。笔者综述了近年来植物天然免疫系统的研究进展,认为随着对植物天然免疫系统研究的深入,应重视PTI和ETI的结合利用,有效扩大植物抗菌谱,改良植物ETI抗性。     

Antimicrobial peptides of multicellular organisms.

Multicellular organisms live, by and large, harmoniously with microbes. The cornea of the eye of an animal is almost always free of signs of infection. The insect flourishes without lymphocytes or antibodies. A plant seed germinates successfully in the midst of soil microbes. How is this accomplished? Both animals and plants possess potent, broad-spectrum antimicrobial peptides, which they use to fend off a wide range of microbes, including bacteria, fungi, viruses and protozoa. What sorts of molecules are they? How are they employed by animals in their defence? As our need for new antibiotics becomes more pressing, could we design anti-infective drugs based on the design principles these molecules teach us?     

The structural basis for activation of plant immunity by bacterial effector protein AvrPto

Pathogenic microbes use effectors to enhance susceptibility in host plants. However, plants have evolved a sophisticated immune system to detect these effectors using cognate disease resistance proteins, a recognition that is highly specific, often elicits rapid and localized cell death, known as a hypersensitive response, and thus potentially limits pathogen growth. Despite numerous genetic and biochemical studies on the interactions between pathogen effector proteins and plant resistance proteins, the structural bases for such interactions remain elusive. The direct interaction between the tomato protein kinase Pto and the Pseudomonas syringae effector protein AvrPto is known to trigger disease resistance and programmed cell death through the nucleotide-binding site/leucine-rich repeat (NBS-LRR) class of disease resistance protein Prf. Here we present the crystal structure of an AvrPto-Pto complex. Contrary to the widely held hypothesis that AvrPto activates Pto kinase activity, our structural and biochemical analyses demonstrated that AvrPto is an inhibitor of Pto kinase in vitro. The AvrPto-Pto interaction is mediated by the phosphorylation-stabilized P+1 loop and a second loop in Pto, both of which negatively regulate the Prf-mediated defences in the absence of AvrPto in tomato plants. Together, our results show that AvrPto derepresses host defences by interacting with the two defence-inhibition loops of Pto.     

Selecting and maintaining a diverse T-cell repertoire

To provide a T-cell population that will respond promptly to foreign antigen, the immune system looks inward, using the variety of self-antigens to select and maintain a diverse repertoire of receptors. A protective immune system must include a T-lymphocyte population that is poised to respond to foreign antigenic peptides presented by self-major histocompatibility complex molecules. As the organism cannot predict the precise pathogen-derived antigens that will be encountered, the system uses the diverse array of self-peptides bound to self-major histocompatibility complex molecules, not only to select a receptor repertoire in the thymus, but also to keep na?ve T cells alive and 'ready for action' in the periphery.     

Intracellular pattern recognition receptors in the host response

The innate immune system relies on its capacity to rapidly detect invading pathogenic microbes as foreign and eliminate them. Indeed, Toll-like receptors are a class of membrane receptors that sense extracellular microbes and trigger anti-pathogen signalling cascades. Recently, intracellular microbial sensors have also been identified, including NOD-like receptors and the helicase-domain-containing antiviral proteins RIG-I and MDA5. Some of these cytoplasmic molecules sense microbial, as well as non-microbial, danger signals, but the mechanisms of recognition used by these sensors remain poorly understood. Nonetheless, it is apparent that these proteins are likely to have critical roles in health and disease.     

Acquisition of a multifunctional IgA+ plasma cell phenotype in the gut

The largest mucosal surface in the body is in the gastrointestinal tract, a location that is heavily colonized by microbes that are normally harmless. A key mechanism required for maintaining a homeostatic balance between this microbial burden and the lymphocytes that densely populate the gastrointestinal tract is the production and transepithelial transport of poly-reactive IgA (ref. 1). Within the mucosal tissues, B cells respond to cytokines, sometimes in the absence of T-cell help, undergo class switch recombination of their immunoglobulin receptor to IgA, and differentiate to become plasma cells. However, IgA-secreting plasma cells probably have additional attributes that are needed for coping with the tremendous bacterial load in the gastrointestinal tract. Here we report that mouse IgA(+) plasma cells also produce the antimicrobial mediators tumour-necrosis factor-α (TNF-α) and inducible nitric oxide synthase (iNOS), and express many molecules that are commonly associated with monocyte/granulocytic cell types. The development of iNOS-producing IgA(+) plasma cells can be recapitulated in vitro in the presence of gut stroma, and the acquisition of this multifunctional phenotype in vivo and in vitro relies on microbial co-stimulation. Deletion of TNF-α and iNOS in B-lineage cells resulted in a reduction in IgA production, altered diversification of the gut microbiota and poor clearance of a gut-tropic pathogen. These findings reveal a novel adaptation to maintaining homeostasis in the gut, and extend the repertoire of protective responses exhibited by some B-lineage cells.     

A saponin-detoxifying enzyme mediates suppression of plant defences

Plant disease resistance can be conferred by constitutive features such as structural barriers or preformed antimicrobial secondary metabolites. Additional defence mechanisms are activated in response to pathogen attack and include localized cell death (the hypersensitive response). Pathogens use different strategies to counter constitutive and induced plant defences, including degradation of preformed antimicrobial compounds and the production of molecules that suppress induced plant defences. Here we present evidence for a two-component process in which a fungal pathogen subverts the preformed antimicrobial compounds of its host and uses them to interfere with induced defence responses. Antimicrobial saponins are first hydrolysed by a fungal saponin-detoxifying enzyme. The degradation product of this hydrolysis then suppresses induced defence responses by interfering with fundamental signal transduction processes leading to disease resistance.     

土壤微生物多样性与植物多样性

土壤中生活着丰富的微生物类群,是一个重要的地下生物宝库.土壤微生物是土壤中的主要分解者,对环境起着天然的“过滤”和“净化”作用,在自然生态系统的功能发挥和维持能力方面极其重要.植物、土壤和微生物相互作用,构成了一个植物-土壤-微生物的有机整体.土壤微生物多样性代表着微生物群落的稳定性,指生命体在遗传、种类和生态系统层次上的变化.从遗传、分类、生态功能以及系统发育等多方面阐述了当前土壤微生物多样性的研究工作.同时探讨了植物多样性与土壤微生物多样性之间的内在联系,植被的破坏可直接导致土壤微生物多样性的丧失,而土壤微生物对植物物种多样性的维持又具有重要作用.因此,加强土壤微生物多样性研究对植物多样性保护具有重要意义.     

Reciprocal interactions of the intestinal microbiota and immune system

The emergence of the adaptive immune system in vertebrates set the stage for evolution of an advanced symbiotic relationship with the intestinal microbiota. The defining features of specificity and memory that characterize adaptive immunity have afforded vertebrates the mechanisms for efficiently tailoring immune responses to diverse types of microbes, whether to promote mutualism or host defence. These same attributes can put the host at risk of immune-mediated diseases that are increasingly linked to the intestinal microbiota. Understanding how the adaptive immune system copes with the remarkable number and diversity of microbes that colonize the digestive tract, and how the system integrates with more primitive innate immune mechanisms to maintain immune homeostasis, holds considerable promise for new approaches to modulate immune networks to treat and prevent disease.     

植物抗病信号传导途径及其相互作用

植物与病原物长期的互作过程中产生了一系列的防卫反应，其中系统获得性抗性(Systemic Acquired Resistance,SAR)和诱导性系统抗性（Induced Systemic Resistance,ISR)是植物抗病信号传导途径中的两 种重要形式。它们分别由植物内源信号分子SA和JA／Et作介导，两种信号的传导途径之间既相互独立相互联系，协同作用，从而使植物出对自身伤害最小却又最有有效的防卫反应。笔就SA－领带性信号传导途径和SA－非领带性信号传导途径的分子生学研究进展，以及两种信号传导途径间的相互作用等方面进行了综述。     

烟草赤星病菌孢子萌发和侵染条件的研究

用烟草赤星病菌两个菌株进行测定,孢子在烟草叶面萌发能力最强;其次是在1％的葡萄糖溶液中;在蒸馏水中萌发最弱。在侵染试验中,用丙酮和70％酒精清洗的幼苗叶片发病加重;露天放置的烟苗较生长在温室内的烟苗发病重。在3种接种方法中,以孢子悬滴法效果最好。侵染和接种方法中的幼苗,其叶面微生物在种类和数量上均以处理的不同而有差别。     

Metabolic priming by a secreted fungal effector

Maize smut caused by the fungus Ustilago maydis is a widespread disease characterized by the development of large plant tumours. U. maydis is a biotrophic pathogen that requires living plant tissue for its development and establishes an intimate interaction zone between fungal hyphae and the plant plasma membrane. U. maydis actively suppresses plant defence responses by secreted protein effectors. Its effector repertoire comprises at least 386 genes mostly encoding proteins of unknown function and expressed exclusively during the biotrophic stage. The U. maydis secretome also contains about 150 proteins with probable roles in fungal nutrition, fungal cell wall modification and host penetration as well as proteins unlikely to act in the fungal-host interface like a chorismate mutase. Chorismate mutases are key enzymes of the shikimate pathway and catalyse the conversion of chorismate to prephenate, the precursor for tyrosine and phenylalanine synthesis. Root-knot nematodes inject a secreted chorismate mutase into plant cells likely to affect development. Here we show that the chorismate mutase Cmu1 secreted by U. maydis is a virulence factor. The enzyme is taken up by plant cells, can spread to neighbouring cells and changes the metabolic status of these cells through metabolic priming. Secreted chorismate mutases are found in many plant-associated microbes and might serve as general tools for host manipulation.     

植物病害生物防治菌的改良技术及产业化

介绍了植病生防菌的遗传改良技术,通过诱变育种、杂交育种及基因工程技术增强生防菌的抗菌活性和扩大防治对象,使改良后的生防菌较传统的生物杀菌剂具有更高的生防效率和更强的市场竞争力,这些改良技术的研究需要现代生物科学、分子生物学等多学科的结合。对生防菌的产业化研究作了综述,分析了生防菌产业化研究现状及实现产业化的关键技术指出了生防菌产业化的市场开发需要国家的支持,科研单位和企业等各方面的合作。     

基于PC机的多客户响应实时数据采集系统

为解决一种基于PC网络的数据采集系统如何响应多个分散客户对实时数据采集的请求问题，建立了一个数据采集端响应的模型，提出了一种利用操作系统的多任务，程序多线程、时间片分隔法以及缓冲区非空触发法等实现上述功能要求的方案，实现了多个客户端实时数据请求的响应，为硬件资源的共享和以数据采集为基础的虚拟仪器的建立提出了一种可响应多用户请求的解决办法。     

IgE-mediated degranulation of mast cells does not require opening of ion channels

Rat peritoneal mast cells respond to antigenic stimulation by releasing histamine through exocytosis. The dynamics of exocytosis can be investigated by dialysing single cells with patch pipettes using the whole-cell recording configuration of the patch-clamp technique. However, dialysed cells fail to respond to external stimuli such as compound 48/80 or antigens, suggesting that essential cytoplasmic components have been washed out. We have developed a new patch-clamp configuration in which the patch under the pipette tip is not disrupted but instead permeabilized, preventing the diffusion of large molecules out of the cell. In this configuration the cell responds to external stimulation, and the capacitance as well as the conductance of the cell membrane can be recorded during degranulation. On antigenic stimulation, the cell capacitance (proportional to plasma membrane area), after an initial delay, increases by a factor of about 3. This increase in capacitance is often preceded by a transient increase in conductance. Agents that block Ca-activated channels inhibit this conductance change without affecting the amplitude and time course of degranulation. We therefore conclude that, in contrast to excitable secretory cells such as chromaffin cells, mast cells do not use ion channels in stimulus-secretion coupling.     

数字滤波器参数的设计

通过调用MATLAB信号处理工具箱函数，实现有限冲激响应数字滤波器(FIR)和无限冲激响应数字滤波器(IIR)的参数的设计，分析了仿真输出幅频响应的图形，同时讨论了FIR和IIR数字滤波器的设计的各自特点。     

Single stretch-activated ion channels in vascular endothelial cells as mechanotransducers?

Endothelial cells line the inner surface of blood vessels and act as the main barrier to the passage of cells and large molecules from the blood stream to the tissues. Recent interest in the part played by the endothelium in regulating vascular tone has focused on the synthesis and secretion of prostacyclin and an endothelium-derived relaxing factor. Endothelial cells respond to blood-borne agonist, but how the endothelium senses and responds to mechanical forces generated by the flow of blood under pressure is not known. Here we report patch-clamp recordings of ion channel activity from cell-attached membrane patches on aortic endothelial cells. In most of the patches examined, we observed unitary inward currents associated with the opening of a cation-selective channel (approximately 40 pS in standard saline). The channel is permeable to Ca2+ and its opening frequency increases when the membrane is stretched by applying suction through the patch electrode. The presence of mechanotransducing ion channels in endothelial cells may help explain how the endothelium mediates vascular responses to haemodynamic stresses.     

Nitrogen limitation of microbial decomposition in a grassland under elevated CO2

Carbon accumulation in the terrestrial biosphere could partially offset the effects of anthropogenic CO2 emissions on atmospheric CO2. The net impact of increased CO2 on the carbon balance of terrestrial ecosystems is unclear, however, because elevated CO2 effects on carbon input to soils and plant use of water and nutrients often have contrasting effects on microbial processes. Here we show suppression of microbial decomposition in an annual grassland after continuous exposure to increased CO2 for five growing seasons. The increased CO2 enhanced plant nitrogen uptake, microbial biomass carbon, and available carbon for microbes. But it reduced available soil nitrogen, exacerbated nitrogen constraints on microbes, and reduced microbial respiration per unit biomass. These results indicate that increased CO2 can alter the interaction between plants and microbes in favour of plant utilization of nitrogen, thereby slowing microbial decomposition and increasing ecosystem carbon accumulation.