低温对植物叶片蛋白质组的影响

低温会影响植物形态与代谢活动,植物应答低温胁迫的生理与分子生物学机制一直是人们关注的热点问题。分析了拟南芥(Arabidopsis thaliana)等7种植物应对低温胁迫的蛋白质组学研究结果,为全面理解植物低温应答机制提供了线索。     

高等植物核型雄性不育的分子机理研究进展

近10年来,雄性不育在杂交育种中得到了广泛运用,它为利用杂种优势对农作物进行轮回选择和群体改良提供了重要工具.同时在生命科学研究中,雄性不育也为花粉发育、细胞质遗传和核质互作的研究提供了重要材料.以前对植物雄性不育的研究多定位于描述性和细胞水平的研究,对其分子机制了解较少.近年来,随着在模式植物中克隆到的与雄性育性有关的突变基因的数量不断增多,对雄性不育的分子机理的研究也逐步深入.迄今已知,在雄配子体及其营养组织的发育、花粉与雌性器官的识别以及随后的双受精过程中,都有相关基因在进行调控.本文针对细胞核雄性不育,按雄性生殖器官发育的顺序,结合分子生物学、细胞学和遗传学研究结果,对高等植物核型雄性不育分子机理的研究进展进行综述.     

骨骼肌肌纤维形成机制的研究进展

骨骼肌是动物躯体最重要的组成部分,占到产肉动物躯体的40%,肌纤维作为骨骼肌组织的主要成分,其类型的差异是影响产肉动物肌肉品质的重要因素之一。因此,骨骼肌的生长发育与产肉动物肉的产量有着密切的联系,而其生理生化特性的差异也将会直接影响到产肉动物屠宰之后肉品的质量。一般而言,动物骨骼肌肌纤维数目在胚胎发育期间基本上就已固定,出生之后,由于肌纤维的肥大,动物躯体肌肉块才表现出增大增粗。另外,动物肌肉块在生长发育过程中,其肌纤维组成类型并不是完全固定的,它们会随着骨骼肌对代谢与功能需求的改变而发生转变。骨骼肌的生长发育,以及骨骼肌肌纤维类型的发生与发展是一个非常复杂的生物学过程,受到许多信号通路与因子的调控。随着分子生物学技术的飞速发展,各种先进技术相继被应用于生物学现象的研究中,利用这些分子生物学技术很好的阐明了许多复杂生物学现象形成的分子机制。目前,骨骼肌生长发育的分子遗传调控机制取得了长足的进展,许多与骨骼肌形成发育相关的关键因子已被鉴定出来。然而,在早期研究中,人们对于骨骼肌肌纤维的研究主要集中在类型的鉴定,以及不同肌纤维类型生理生化特性的分析,对于骨骼肌肌纤维形成的具体分子遗传调控机制的研究相对较少。近年来,随着研究的不断深入,骨骼肌肌纤维形成的分子遗传调控机制也取得了突破性的进展。因此,有必要进一步对骨骼肌肌纤维类型的特性,骨骼肌肌纤维类型形成的分子机制,以及肌纤维类型与肌肉品质的关系进行全面的综述。本文首先对肌纤维的类型、特性进行了综述;进一步分别对慢型肌纤维与快型肌纤维形成的分子调控机制的研究进展进行了回顾;最后对肌纤维类型与肉品质的关系进行了讨论。总之,本综述的撰写将有助于对骨骼肌肌纤维类型形成的遗传机制的进一步了解,为将来进一步的深入研究肌纤维形成的分子机制提供参考;同时也将有助于揭示肌肉品质形成的分子遗传调控机制,为利用分子生物学技术培育高品质新品种或新品系产肉动物提供分子理论依据。     

水稻白叶枯病菌致病性分子遗传学基础

 水稻-白叶枯病原菌互作符合基因对基因关系，是研究禾本科植物-病原菌互作的理想模式系统。目前已鉴定和克隆出许多白叶枯病菌致病相关基因。其它革兰氏阴性植物病原细菌致病性分子遗传学和基因组学研究，为揭示水稻白叶枯病菌致病性分子机理提供了丰富的背景知识，其中以发掘TTSS效应分子的研究备受关注。本文将对白叶枯病菌致病性分子机理进行综述，以期为研究水稻-白叶枯病菌互作的功能基因组学提供科学线索。     

真菌细胞自噬的研究进展

为了维持细胞内部物质与能量的动态平衡,真菌在进化过程中形成了一些复杂的机制来调控胞内物质的代谢和循环,其中的一条重要途径就是自噬。自噬在真核生物体内是高度保守的,其通过形成具有双层膜结构的自噬体囊泡,将细胞内受损的细胞器或蛋白质包裹起来,随后运输到液泡中进行降解。在过去20多年里,人们对真菌细胞自噬进行了深入的研究,通过对自噬相关蛋白的分析,逐渐揭示了自噬过程中的一些分子及调控机制。在对丝状真菌自噬基因功能分析的过程中,发现自噬在丝状真菌营养生长、产孢、孢子萌发、侵染结构形成以及致病力等方面都起着非常重要的作用。本综述介绍了真菌细胞自噬的分子及调控机制以及自噬基因在丝状真菌中的功能的研究进展。     

Molecular genetics: applications to the clinical neurosciences

Application of molecular biology, by means of linkage analysis and DNA probes that demonstrate restriction fragment length polymorphisms (RFLPs), has resulted in the chromosomal localization of the genes responsible for a number of neurological disorders. Characterization of the structure and function of individual genes for these diseases is in an early stage, but information available indicates that the molecular mechanisms underlying phenotypic expression of neurological diseases encompass a wide range of genetic errors ranging from the most minor (a single-base pair mutation) to large chromosomal deletions. Linkage analysis can now be used for genetic counseling in several of these disorders.     

Deciphering the cross-talk of implantation: advances and challenges

Implantation involves a series of steps leading to an effective reciprocal signaling between the blastocyst and the uterus. Except for a restricted period when ovarian hormones induce a uterine receptive phase, the uterus is an unfavorable environment for blastocyst implantation. Because species-specific variations in implantation strategies exist, these differences preclude the formulation of a unifying theme for the molecular basis of this event. However, an increased understanding of mammalian implantation has been gained through the use of the mouse model. This review summarizes recognized signaling cascades and new research in mammalian implantation, based primarily on available genetic and molecular evidence from implantation studies in the mouse. Although the identification of new molecules associated with implantation in various species provides valuable insight, important questions remain regarding the common molecular mechanisms that govern this process. Understanding the mechanisms of implantation promises to help alleviate infertility, enhance fetal health, and improve contraceptive design. The success of any species depends on its reproductive efficiency. For sexual reproduction, an egg and sperm must overcome many obstacles to fuse and co-mingle their genetic material at fertilization. The zygote develops into a blastocyst with two cell lineages (the inner cell mass and the trophectoderm), migrates within the reproductive tract, and ultimately implants into a transiently permissive host tissue, the uterus. However, the molecular basis of the road map connecting the blastocyst with the endometrium across species is diverse (1) and not fully understood. Recent advances have identified numerous molecules involved in implantation (1-4), yet new discoveries have not yielded a unifying scheme for the mechanisms of implantation.     

藻类响应环境胁迫的蛋白质组变化研究进展

环境变化会影响植物的生长与代谢。近来,藻类植物应答环境胁迫的蛋白质组学研究已成为热点。整合分析了藻类植物应答各种环境胁迫(盐、重金属、温度、光和营养元素等)的蛋白质组学研究结果,为全面理解藻类植物响应环境胁迫的代谢调控机制提供了重要的信息。     

Electron transfer: classical approaches and new frontiers

Electron transfer, under conditions of weak interaction and a medium acting as a passive thermal bath, is very well understood. When electron transfer is accompanied by transient chemical bonding, such as in interfacial coordination electrochemical mechanisms, strong interaction and molecular selectivity are involved. These mechanisms, which take advantage of "passive self-organization," cannot yet be properly described theoretically, but they show substantial experimental promise for energy conversion and catalysis. The biggest challenge for the future, however, may be dynamic, self-organized electron transfer. As with other energy fluxes, a suitable positive feedback mechanism, through an active molecular environment, can lead to a (transient) decrease of entropy equivalent to an increase of molecular electronic order for the activated complex. A resulting substantial increase in the rate of electron transfer and the possibility of cooperative transfer of several electrons (without intermediates) can be deduced from phenomenological theory. The need to extend our present knowledge may be derived from the observation that chemical syntheses and fuel utilization in industry typically require high temperatures (where catalysis is less relevant), whereas corresponding processes in biological systems are catalyzed at environmental conditions. This article therefore focuses on interfacial or membrane-bound electron transfer and investigates an aspect that nature has developed to a high degree of perfection: self-organization.     

New paradigms in type 2 immunity

Nearly half of the world's population harbors helminth infections or suffers from allergic disorders. A common feature of this population is the so-called "type 2 immune response," which confers protection against helminths, but also promotes pathologic responses associated with allergic inflammation. However, the mechanisms that initiate and control type 2 responses remain enigmatic. Recent advances have revealed a role for the innate immune system in orchestrating type 2 responses against a bewildering array of stimuli, from nanometer-sized allergens to 20-meter-long helminth parasites. Here, we review these advances and suggest that the human immune system has evolved multiple mechanisms of sensing such stimuli, from recognition of molecular patterns via innate immune receptors to detecting metabolic changes and tissue damage caused by these stimuli.     

Symmetry breaking and the evolution of development

Because of its simplicity, the binary-switch nature of left-right asymmetry permits meaningful comparisons among many different organisms. Phylogenetic analyses of asymmetry variation, inheritance, and molecular mechanisms reveal unexpected insights into how development evolves. First, directional asymmetry, an evolutionary novelty, arose from nonheritable origins almost as often as from mutations, implying that genetic assimilation ("phenotype precedes genotype") is a common mode of evolution. Second, the molecular pathway directing hearts leftward-the nodal cascade-varies considerably among vertebrates (homology of form does not require homology of development) and was possibly co-opted from a preexisting asymmetrical chordate organ system. Finally, declining frequencies of spontaneous asymmetry reversal throughout vertebrate evolution suggest that heart development has become more canalized.     

New directions in neuronal migration

Over the past decade, genetic analyses have yielded a more molecular view of neuronal migration and its role in central nervous system development. We now realize that many of the molecular mechanisms that guide migrations in invertebrates are recapitulated in the vertebrate nervous system. These mechanisms guide dorsoventral and anterior-posterior migrations and merge with radial migratory pathways that are prominent in the development of the mammalian cortex. This review discusses the choreography of these different migratory mechanisms within the context of genetic approaches that have defined their molecular mechanisms.     

动物遗传育种学科百年发展历程与研究前沿

经过上万年的野生物种驯化、自然选择和人工选择,世界各国逐渐形成了现有的家养动物品种。伴随着遗传学理论的发现和逐步完善,动物常规育种技术从一般的表型选择发展到利用BLUP方法进行育种值估计,在近五十年为畜禽遗传改良做出了巨大贡献。20世纪80年代,各种分子遗传标记的逐步问世和现代生物技术的迅速发展为动物遗传育种工作的研究和改良提供了新的途径和方法。DNA、RNA、蛋白质等各种组学信息的整合研究,不但为动物重要经济性状功能基因挖掘、分子遗传机制解析带来新的契机,并且使得动物育种从传统育种时代真正迈入分子育种时代。近年来,世界动物育种工作在分子数量遗传学、功能基因组学、分子育种技术等方面都取得了显著进展。     

Crystal structure of defensin HNP-3, an amphiphilic dimer: mechanisms of membrane permeabilization

Defensins (molecular weight 3500 to 4000) act in the mammalian immune response by permeabilizing the plasma membranes of a broad spectrum of target organisms, including bacteria, fungi, and enveloped viruses. The high-resolution crystal structure of defensin HNP-3 (1.9 angstrom resolution, R factor 0.19) reveals a dimeric beta sheet that has an architecture very different from other lytic peptides. The dimeric assembly suggests mechanisms by which defensins might bind to and permeabilize the lipid bilayer.     

植物热激蛋白响应非生物胁迫研究进展

非生物胁迫对农作物正常生长具有重要影响,非生物胁迫可改变细胞蛋白质构象,使非天然蛋白 质发生聚集,破坏细胞膜结构。热激蛋白（heat shock proteins,Hsps）负责蛋白质的折叠、组装、转运与降解, 并能在胁迫条件下协助蛋白质复性,通过重建正常的蛋白质构象从而恢复细胞稳态,参与其他应激反应机制, 在保护植物免受非生物胁迫方面起着重要作用。总结了各类 Hsps 在植物非生物胁迫响应中发挥的功能,阐述 Hsps 参与其他应激反应机制并发挥一定作用,对目前 Hsps 在研究中存在的问题进行讨论和展望,为作物分子育 种筛选抗逆基因提供理论依据。     

Research advance on the physiologically molecular mechanisms for plant heavy metal tolerance

植物可以通过一系列动态的分子生理机制来减少重金属的胁迫 这些机制包括重金属离子与细胞壁的结合 ,限制重金属离子透过细胞膜 ,重金属离子或化合物的排出 ,重金属在植物体内的转移 ,重金属的络合与区隔化以及植物对胁迫的基本的反应机制如胁迫蛋白含量的变化等 本文就植物耐重金属的分子生理机制进行综述     

植物耐重金属分子生理机制研究进展

植物可以通过一系列动态的分子生理机制来减少重金属的胁迫.这些机制包括重金属离子与细胞壁的结合,限制重金属离子透过细胞膜,重金属离子或化合物的排出,重金属在植物体内的转移,重金属的络合与区隔化以及植物对胁迫的基本的反应机制如胁迫蛋白含量的变化等.本文就植物耐重金属的分子生理机制进行综述.     

The way things move: looking under the hood of molecular motor proteins

The microtubule-based kinesin motors and actin-based myosin motors generate motions associated with intracellular trafficking, cell division, and muscle contraction. Early studies suggested that these molecular motors work by very different mechanisms. Recently, however, it has become clear that kinesin and myosin share a common core structure and convert energy from adenosine triphosphate into protein motion using a similar conformational change strategy. Many different types of mechanical amplifiers have evolved that operate in conjunction with the conserved core. This modular design has given rise to a remarkable diversity of kinesin and myosin motors whose motile properties are optimized for performing distinct biological functions.     

A general model of prion strains and their pathogenicity

Prions are lethal mammalian pathogens composed of aggregated conformational isomers of a host-encoded glycoprotein and which appear to lack nucleic acids. Their unique biology, allied with the public-health risks posed by prion zoonoses such as bovine spongiform encephalopathy, has focused much attention on the molecular basis of prion propagation and the "species barrier" that controls cross-species transmission. Both are intimately linked to understanding how multiple prion "strains" are encoded by a protein-only agent. The underlying mechanisms are clearly of much wider importance, and analogous protein-based inheritance mechanisms are recognized in yeast and fungi. Recent advances suggest that prions themselves are not directly neurotoxic, but rather their propagation involves production of toxic species, which may be uncoupled from infectivity.     

Widespread parallel evolution in sticklebacks by repeated fixation of Ectodysplasin alleles

Major phenotypic changes evolve in parallel in nature by molecular mechanisms that are largely unknown. Here, we use positional cloning methods to identify the major chromosome locus controlling armor plate patterning in wild threespine sticklebacks. Mapping, sequencing, and transgenic studies show that the Ectodysplasin (EDA) signaling pathway plays a key role in evolutionary change in natural populations and that parallel evolution of stickleback low-plated phenotypes at most freshwater locations around the world has occurred by repeated selection of Eda alleles derived from an ancestral low-plated haplotype that first appeared more than two million years ago. Members of this clade of low-plated alleles are present at low frequencies in marine fish, which suggests that standing genetic variation can provide a molecular basis for rapid, parallel evolution of dramatic phenotypic change in nature.