植物细胞程序性死亡的分类和膜通透性调控蛋白研究进展

程序性细胞死亡是由基因调控的贯穿于真核细胞生理和发育过程的细胞自杀行为。动物细胞的程序性死亡分成3类凋亡、自噬和坏死;线粒体和溶酶体分别在前两个过程中起关键作用。关于植物细胞程序性死亡的分类还存在很多争议,焦点是植物是否有细胞凋亡这种形式,核心问题是植物细胞的线粒体外膜上没有Bcl-2家族的膜通透性调控蛋白。近年,程序性细胞死亡也在细菌中发现,LrgAB家族的膜通透性调控蛋白起着重要作用。最近的研究表明,植物叶绿体外被膜上也有LrgAB家族的同源蛋白,它们在控制叶绿体发育和程序性细胞死亡方面起重要作用。因此,叶绿体在植物细胞死亡调控中的作用应该更加受到关注。     

我国科学家在程序性细胞死亡机制研究领域取得重大突破

程序性细胞死亡在调控植物发育和胁迫响应中具有重要作用, 而活性氧是导致程序性细胞死亡的关键因子。日前, 中科院遗传与发育所李家洋研究组对活性氧调控程序性细胞死亡的分子机制进行了深度解析, 首次阐明了苹果酸作为信号分子, 经由叶绿体-线粒体穿梭途径而引发活性氧产生, 继而导致细胞死亡。该研究成果是程序性细胞死亡调控机制领域的重大突破。     

植物细胞程序性死亡中的类caspases蛋白酶

细胞程序性死亡对于植物的正常生长发育及病理过程具有十分重要的生物学意义。现有的实验证据表明,细胞程序性死亡在动物和植物中有许多相似之处,但也各有特点。在植物中,VPEs、metacaspases和saspases等酶类在细胞程序性死亡过程中发挥了关键性作用。该文详细比较了动、植物细胞程序性死亡的差异,并阐述TVPEs、metacaspases和saspases三种类caspases蛋白酶在植物程序性细胞死亡中所起的作用。     

植物细胞程序性死亡中的类caspases 蛋白酶

细胞程序性死亡对于植物的正常生长发育及病理过程具有十分重要的生物学意义。现有的实验证据表明, 细胞程序性死亡在动物和植物中有许多相似之处, 但也各有特点。在植物中, VPEs、metacaspases和saspases 等酶类在细胞程序 性死亡过程中发挥了关键性作用。该文详细比较了动、植物细胞程序性死亡的差异, 并阐述了VPEs 、metacas pases 和saspases三种类caspases蛋白酶在植物程序性细胞死亡中所起的作用。     

植物受体激酶BAK1介导的细胞死亡调控研究进展

植物在生长发育和抵抗逆境时都会发生细胞程序性死亡,植物受体激酶在细胞死亡调控中发挥着十分重要的作用。植物细胞可以通过质膜表面的受体激酶感受细胞间及环境信号,并将信号传递到下游,诱导一系列级联反应,导致细胞程序性死亡。植物受体激酶BAK1在植物程序性死亡中发挥着关键的作用, BAK1与BRI1、FLS2、BIR1、EFR、BIK1等受体激酶互作,识别和转导胞外信号,共同调控细胞死亡。该文以BAK1为中心,综述了近年发现的参与植物细胞死亡调控的BAK1受体激酶复合物介导的信号转导机制,并提出需要深入研究的科学问题。     

与程序性细胞死亡有关的基因

程序性细胞死亡是在基因控制下细胞的主动死亡,存在主动合成蛋白质的过程。研究发现许多与程序性细胞死亡有关的基因,可分为对程序性细胞死亡有促进作用的基因,抑制程序性细胞死亡的基因和协助程序性细胞死亡完成的基因。     

植物细胞程序性死亡研究进展

植物细胞死亡分为坏死和程序性死亡。细胞程序性死亡是具有信号或一系列分子参与,并且由细胞内在的死亡程序介导的有序过程。它在植物生长发育和抵御外界胁迫中具有重要作用。简要介绍了植物PCD的特征,对植物PCD中的信号分子和类caspase的作用等进行了综述,并对植物PCD存在的问题进行分析和展望,为深入研究植物PCD提供参考。     

细胞程序性死亡的非Caspase依赖型途径

程序性细胞死亡是一种程序化的主动性细胞死亡,半胱胺酸天冬氨酸特异性蛋白酶家族(在该过程中起着不可忽视的作用.基于Caspase在程序性细胞死亡过程中所起的作用,将程序性细胞死亡分为两大类:Caspase依赖型和Caspase非依赖型.前者即典型的凋亡,后者包括自体吞噬、副凋亡、有丝分裂灾变、凋亡样程序性死亡、坏死样程序性死亡等.这些Caspase非依赖型的细胞程序性死亡途径与生理及病理现象密切相关.     

活性氧对植物自噬调控的研究进展

自噬是一种在真核生物中高度保守的降解细胞组分的生物过程, 在饥饿、衰老和病菌感染等过程中起关键作用。而活性氧是有氧生物在正常或胁迫条件下产生的一种代谢副产物, 在植物的生长发育、胁迫适应和程序性细胞死亡过程中起重要作用。最新研究结果表明, 当植物受到病菌感染产生超敏反应时活性氧和自噬在程序性细胞死亡、生长发育和胁迫适应过程中起重要调控作用。因此, 该文结合最新的研究进展, 从活性氧的种类及特点、自噬的分子基础以及活性氧在植物自噬中的作用等方面, 探讨了活性氧与植物自噬之间的信号转导关系。     

程序性细胞死亡及其激光FCM检测方法

程序性细胞死亡是细胞生理性死亡最常见的形式,是细胞对其周围环境信号的主动反应。在此过程中细胞发生一系列特征性的变化,一些基因表达参与或调控此过程。ＦＣＭ是检测研究程序性细胞死亡的重要手段。诱导肿瘤细胞发生程序性死亡是肿瘤治疗的新途径。程序性细胞死亡的检测对肿瘤治疗研究及其临床疗效判断都有其应用前景。     

环境因子诱导的植物细胞程序性死亡

细胞发生程序性死亡（Programmed cell death,PCD）是多细胞生物用以消除多余的或有害的细胞的一种重要方式。对于植物个体来说,细胞发生程序性死亡（PCD）是抵抗逆境的一种十分有效的途径。因此,揭示环境因子诱导的植物PCD现象的分子本质就具有十分重要的现实意义。近十年来,有关环境因子诱导的植物PCD研究报道逐年增加。本文重点综述了环境因子与植物PCD相关的研究进展,并对植物PCD的主要生物学意义和研究展望进行了讨论。     

Classes of programmed cell death in plants, compared to those in animals

Relatively little is known about programmed cell death (PCD) in plants. It is nonetheless suggested here that tonoplast rupture and the subsequent rapid destruction of the cytoplasm can distinguish two large PCD classes. One class, which is here called 'autolytic', shows this feature, whilst the second class (called 'non-autolytic') can include tonoplast rupture but does not show the rapid cytoplasm clearance. Examples of the 'autolytic' PCD class mainly occur during normal plant development and after mild abiotic stress. The 'non-autolytic' PCD class is mainly found during PCD that is due to plant-pathogen interactions. Three categories of PCD are currently recognized in animals: apoptosis, autophagy, and necrosis. An attempt is made to reconcile the recognized plant PCD classes with these groups. Apoptosis is apparently absent in plants. Autophagic PCD in animals is defined as being accompanied by an increase in the number of autophagosomes, autolysosomes, and small lytic vacuoles produced by autolysosomes. When very strictly adhering to this definition, there is no (proof for) autophagic PCD in plants. Upon a slightly more lenient definition, however, the 'autolytic' class of plant PCD can be merged with the autophagic PCD type in animal cells. The 'non-autolytic' class of plant PCD, as defined here, can be merged with necrotic PCD in animals.     

Polyamines are common players in different facets of plant programmed cell death

Programmed cell death (PCD) is a process that occurs throughout the life span of every plant life, from initial germination of the seed to the senescence of the plant. It is a normal physiological milestone during the plant’s developmental process, but it can also be induced by external factors, including a variety of environmental stresses and as a response to pathogen infections. Changes in the morphology of the nucleus is one of the most noticeable during PCD but all the components of the plant cell (cytoplasm, cytoskeleton and organelles) are involved in this fascinating process. To date, relatively little is known about PCD in plants, but several factors, among which polyamines (PAs) and plant growth regulators, have been shown to play an important role in the initiation and regulation of the process. The role of PAs in plant PCD appears to be multifaceted acting in some instances as pro-survival molecules, whereas in others seem to be implicated in accelerating PCD. The molecular mechanism is still under study. Here we present some PCD plant models, focusing on the role of the enzyme responsible for PA conjugation to proteins: transglutaminase (TGase), an enzyme linked with the process of PCD also in some animal models. The role of PAs and plant TGase in the senescence and PCD in flowers, leaf and the self-incompatibility of pollen will be discussed and examined in depth.     

Multiple mediators of plant programmed cell death: interplay of conserved cell death mechanisms and plant-specific regulators

Programmed cell death (PCD) is a process aimed at the removal of redundant, misplaced, or damaged cells and it is essential to the development and maintenance of multicellular organisms. In contrast to the relatively well-described cell death pathway in animals, often referred to as apoptosis, mechanisms and regulation of plant PCD are still ill-defined. Several morphological and biochemical similarities between apoptosis and plant PCD have been described, including DNA laddering, caspase-like proteolytic activity, and cytochrome c release from mitochondria. Reactive oxygen species (ROS) have emerged as important signals in the activation of plant PCD. In addition, several plant hormones may exert their respective effects on plant PCD through the regulation of ROS accumulation. The possible plant PCD regulators discussed in this review are integrated in a model that combines plant-specific regulators with mechanisms functionally conserved between animals and plants.     

植物程序性细胞死亡检测技术

程序性细胞死亡(PCD)是细胞死亡的方式之一,在植物发育及逆境响应等方面起着重要作用。主要介绍检测植物PCD的细胞学、生物化学、分子生物学及生理学方法,以及流式细胞仪在植物PCD检测中的应用。 Abstract:Programmed cell death (PCD) is an active way for plant cells marching to death,which plays an important role in plant development and stress responses.Cytological,biochemical,molecular and physiological methods for measuring plant PCD were reviewed.Application of flow cytometer to plant PCD research was also covered.     

Developmental programmed cell death in plants

Mechanisms of plant developmental programmed cell death (PCD) have been intensively studied in recent years. Most plant developmental PCD is triggered by plant hormones, and the 'death signal' may be transduced by hormonal signaling pathways. Although there are some fundamental differences in the regulation of developmental PCD in various eukaryotes of different kingdoms, hormonal control and death signal transduction via pleiotropic signaling pathways constitute a common framework. However, plants possess a unique process of PCD execution that depends on vacuolar lytic function. Comparisons of the developmental PCD mechanisms of plants and other organisms are providing important insights into the detailed characteristics of developmental PCD in plants.     

细胞程序性死亡在植物适应逆境中的意义

细胞程序性死亡是近年来生命科学的研究热点之一,它不仅在植物生长发育中起重要作用,而且与植物适应逆境也密切相关。本文就细胞程序性死亡在植物适应逆境中的重要作用进行了综述,以期对细胞程序性死亡的研究进一步深入和对植物适应逆境的潜力有新的认识。     

环境因子诱导的植物细胞程序性死亡

细胞发生程序性死亡(Programmed cell death,PCD)是多细胞生物用以消除多余的或有害的细胞的一种重要方式。对于植物个体来说,细胞发生程序性死亡(PCD)是抵抗逆境的一种十分有效的途径。因此,揭示环境因子诱导的植物PCD现象的分子本质就具有十分重要的现实意义。近十年来,有关环境因子诱导的植物PCD研究报道逐年增加。本文重点综述了环境因子与植物PCD相关的研究进展,并对植物PCD的主要生物学意义和研究展望进行了讨论。     

Many ways to exit? Cell death categories in plants

Programmed cell death (PCD) is an integral part of plant development and defence. It occurs at all stages of the life cycle, from fertilization of the ovule to death of the whole plant. Without it, tall trees would probably not be possible and plants would more easily succumb to invading microorganisms. Here, we have attempted to categorize plant PCD in relation to three established morphological types of metazoan cell death: apoptosis, autophagy and non-lysosomal PCD. We conclude that (i) no examples of plant PCD conform to the apoptotic type, (ii) many examples of PCD during plant development agree with the autophagic type, and (iii) that other examples are apparently neither apoptotic nor autophagic.     

Anti-apoptotic machinery protects the necrotrophic fungus Botrytis cinerea from host-induced apoptotic-like cell death during plant infection

Necrotrophic fungi are unable to occupy living plant cells. How such pathogens survive first contact with living host tissue and initiate infection is therefore unclear. Here, we show that the necrotrophic grey mold fungus Botrytis cinerea undergoes massive apoptotic-like programmed cell death (PCD) following germination on the host plant. Manipulation of an anti-apoptotic gene BcBIR1 modified fungal response to PCD-inducing conditions. As a consequence, strains with reduced sensitivity to PCD were hyper virulent, while strains in which PCD was over-stimulated showed reduced pathogenicity. Similarly, reduced levels of PCD in the fungus were recorded following infection of Arabidopsis mutants that show enhanced susceptibility to B. cinerea. When considered together, these results suggest that Botrytis PCD machinery is targeted by plant defense molecules, and that the fungal anti-apoptotic machinery is essential for overcoming this host-induced PCD and hence, for establishment of infection. As such, fungal PCD machinery represents a novel target for fungicides and antifungal drugs.