植物在逆境胁迫中的细胞程序性死亡

细胞程序性死亡(programmed cell death,PCD)是一种由基因控制的、主动的细胞死亡过程,它对植物正常生长发育起重要作用.在逆境胁迫因子如病原体、高盐、低氧、低温、热激和金属离子等作用下,植物为了抵御不良环境的侵害,以活性氧、Ca2+、乙烯和NO等为信号因子,诱导植物体的特定部位发生PCD,形成细胞主动死亡,从而避免逆境对其他组织进一步伤害,并使植物获得对不良环境的适应性.对植物PCD的一般特征、环境胁迫因子及诱导PCD信号分子等进行了综述,为在逆境条件下深入研究植物细胞程序性死亡提供参考.     

浮游植物中一氧化氮的生理作用研究进展

一氧化氮（NO）作为一种具有生物活性的气体自由基分子,它的功能代表了生物学系统中信号传递的新途径。大量证据表明,NO在浮游植物细胞中的功能和在高等动植物中类似,具有调节生长和参与抗逆性的作用,NO和ROS可能作为信号分子参与介导浮游植物程序性死亡（PCD）过程。文章较全面地介绍了NO在浮游植物中的产生途径、测定方法、生理功能和PCD的关系及作为信号分子的作用,并对该领域今后的研究进行了展望。     

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。     

环境胁迫诱导的植物细胞程序性死亡

在最近的10年中,兴起了对植物细胞程序性死亡的研究。大量的证据表明,在各种环境胁迫因子诱导植物细胞PCD过程中,活性氧、乙烯、Ca2+、水杨酸、NO等成为重要的信号分子。像动物细胞凋亡一样,在植物PCD中也存在一条依赖于天冬氨酸特异性半胱氨酸蛋白酶(Caspases)活性的信号传导途径,其中,线粒体处于PCD调控的中心位置。 Abstract:Programmed cell death (PCD) research in higher plants has blossomed in the past ten years.Many evidences suggested that reactive oxygen species,ethylene,Ca2+,salicylic acid,nitric oxide etc.are important signal molecules during environmental stress-induced PCD in plants.Like apoptosis in animals,there also exists a Caspase-dependent PCD signal transduction pathway,in which mitochondrion plays a role of central depot.     

独脚金内酯对单针藻油脂积累的影响

文章研究了独脚金内酯(Strigolactone, SL)对单针藻Monoraphidium sp. QLY-1生长、油脂积累、生理指标和与油脂合成相关酶活性的影响,探讨了SL对藻细胞内信号分子活性氧(ROS)、一氧化氮(NO)和Ca2+与油脂合成的关系。结果表明,在1μmol/L SL诱导条件下,其油脂含量可达48.76%,比对照组(38.12%)提高了27.91%。此外, SL提高了胞内Ca2+、NO水平、乙酰辅酶A羧化酶(ACC)和苹果酸酶(ME)的活性,同时下调了ROS和磷酸式烯醇式丙酮酸(PEPC)的活性。研究表明, SL促进单针藻积累油脂与调控胞内信号分子水平和油脂合成关键酶活性有关,为利用SL诱导微藻积累油脂提供了一定的理论基础。     

液泡信号通路依赖的细胞程序性死亡研究进展

液泡是植物细胞专一性器官之一,具有多种功能,参与细胞内环境调节和细胞解毒等过程。研究表明,液泡在植物细胞程序性死亡（programmed cell death,PCD）中具有重要作用。在液泡介导的PCD过程中,液泡加工酶（vacuolar processing enzyme,VPE）的调控和激活是PCD的关键环节。着眼于液泡信号通路依赖的PCD,对相关细胞事件和分子调控机制进行了讨论,并对未来的研究方向作了展望,以期能推进PCD机制解明。     

NO体外供体硝普钠诱导蚕豆气孔保卫细胞死亡机理研究

为分析NO在植物细胞死亡过程中的作用,以蚕豆表皮条和NO体外供体硝普钠(SNP)及NO信号途径抑制剂为材料,采用表皮条生物法,探讨SNP对蚕豆叶面保卫细胞的毒性机理.结果表明:(1)0.5～9 mmol· L-1的SNP可使蚕豆气孔保卫细胞活性降低,部分细胞死亡,且随着SNP浓度的增高细胞死亡率增高.(2)凋亡抑制剂Z-Asp-CH2-DCB或TLCK可显著降低SNP诱发的保卫细胞死亡率.(3)抗坏血酸(AsA)、过氧化氢酶(CAT)、Ca2+螯合剂EGTA或Ca2+通道抑制剂LaCl3与SNP共同作用时,细胞死亡率显著降低.(4)NO清除剂c-PTIO、MAPK激酶抑制剂PD98059和鸟苷酸环化酶抑制荆ODQ亦能有效阻止SNP诱发的细胞死亡.研究发现,较高浓度的SNP可诱导蚕豆保卫细胞程序性死亡,SNP诱发植物细胞死亡与胁迫组保卫细胞内NO、ROS和Ca2+水平升高有关,cGMP和MAPK参与了SNP诱发的细胞死亡.     

褪黑素对非生物胁迫下雨生红球藻中虾青素积累的影响

以雨生红球藻Haematococcus pluvialis LUGU株为研究对象, 研究在高光照和缺氮胁迫条件下, 添加不同浓度褪黑素(melatonin, MLT)对雨生红球藻生长、虾青素积累、活性氧(ROS)、信号分子及dxs基因表达量的影响。结果表明, 外源添加10 μmol/L MLT可有效提高藻细胞中虾青素的含量, 最高可达31.32 mg/g, 是对照组(13.27 mg/g)的2.36倍; 抑制了细胞内ROS水平, 上调了信号分子一氧化氮(NO)和水杨酸(SA)的含量; 此外, dxs基因表达水平比对照组明显提高, 最高达11.3倍。研究表明, 在非生物胁迫条件下, 雨生红球藻中虾青素的大量积累可能与外源MLT调控细胞内ROS、信号分子及基因表达有关。     

镉诱导拟南芥细胞程序性死亡过程中NO产生和亚细胞定位观察

镉是一种高度有毒的重金属,能够抑制植物生长,甚至导致死亡,但是其诱导细胞程序性死亡(PCD)的分子机制仍然不是很清楚。本文利用荧光探针分子成像和激光共聚焦扫描显微技术,以拟南芥叶肉细胞原生质体为材料,观察100μmol/L CdCl2诱导PCD过程中一氧化氮(NO)的产生和亚细胞定位。结果表明高浓度CdCl2能够明显降低细胞活力,100μmol/L CdCl2能够诱导大量NO产生,在处理12 h后NO产生达到峰值。亚细胞定位观察发现NO荧光首先和线粒体有共定位。随着处理时间的延长在叶绿体和胞质也观察到NO荧光。     

植物过氧化物酶体在活性氧信号网络中的作用

过氧化物酶体是高度动态、代谢活跃的细胞器,主要参与脂肪酸等脂质的代谢及产生和清除不同的活性氧(reactive oxygen species, ROS)。ROS是细胞有氧代谢的副产物。当胁迫长期作用于植物,过量的ROS会引起氧胁迫,损害细胞结构和功能的完整性,导致细胞代谢减缓,活性降低,甚至死亡;但低浓度的ROS则作为分子信号,感应细胞ROS/氧化还原变化,从而触发由环境因素导致的过氧化物酶体动力学以及依赖ROS信号网络改变而产生快速、特异性的应答。ROS也可以通过直接或间接调节细胞生长来控制植物的发育,是植物发育的重要调节剂。此外,过氧化物酶体的动态平衡由ROS、过氧化物酶体蛋白酶及自噬过程调节,对于维持细胞的氧化还原平衡至关重要。本文就过氧化物酶体中ROS的产生和抗氧化剂的调控机制进行综述,以期为过氧化物酶体如何感知环境变化,以及在细胞应答中,ROS作为重要信号分子的研究提供参考。     

Changes in the antioxidant systems as part of the signaling pathway responsible for the programmed cell death activated by nitric oxide and reactive oxygen species in tobacco Bright-Yellow 2 cells

Nitric oxide (NO) has been postulated to be required, together with reactive oxygen species (ROS), for the activation of the hypersensitive reaction, a defense response induced in the noncompatible plant-pathogen interaction. However, its involvement in activating programmed cell death (PCD) in plant cells has been questioned. In this paper, the involvement of the cellular antioxidant metabolism in the signal transduction triggered by these bioactive molecules has been investigated. NO and ROS levels were singularly or simultaneously increased in tobacco (Nicotiana tabacum cv Bright-Yellow 2) cells by the addition to the culture medium of NO and/or ROS generators. The individual increase in NO or ROS had different effects on the studied parameters than the simultaneous increase in the two reactive species. NO generation did not cause an increase in phenylalanine ammonia-lyase (PAL) activity or induction of cellular death. It only induced minor changes in ascorbate (ASC) and glutathione (GSH) metabolisms. An increase in ROS induced oxidative stress in the cells, causing an oxidation of the ASC and GSH redox pairs; however, it had no effect on PAL activity and did not induce cell death when it was generated at low concentrations. In contrast, the simultaneous increase of NO and ROS activated a process of death with the typical cytological and biochemical features of hypersensitive PCD and a remarkable rise in PAL activity. Under the simultaneous generation of NO and ROS, the cellular antioxidant capabilities were also suppressed. The involvement of ASC and GSH as part of the transduction pathway leading to PCD is discussed.     

Arabidopsis ACCELERATED CELL DEATH2 modulates programmed cell death

The Arabidopsis thaliana chloroplast protein ACCELERATED CELL DEATH2 (ACD2) modulates the amount of programmed cell death (PCD) triggered by Pseudomonas syringae and protoporphyrin IX (PPIX) treatment. In vitro, ACD2 can reduce red chlorophyll catabolite, a chlorophyll derivative. We find that ACD2 shields root protoplasts that lack chlorophyll from light- and PPIX-induced PCD. Thus, chlorophyll catabolism is not obligatory for ACD2 anti-PCD function. Upon P. syringae infection, ACD2 levels and localization change in cells undergoing PCD and in their close neighbors. Thus, ACD2 shifts from being largely in chloroplasts to partitioning to chloroplasts, mitochondria, and, to a small extent, cytosol. ACD2 protects cells from PCD that requires the early mitochondrial oxidative burst. Later, the chloroplasts of dying cells generate NO, which only slightly affects cell viability. Finally, the mitochondria in dying cells have dramatically altered movements and cellular distribution. Overproduction of both ACD2 (localized to mitochondria and chloroplasts) and ascorbate peroxidase (localized to chloroplasts) greatly reduces P. syringae-induced PCD, suggesting a pro-PCD role for mitochondrial and chloroplast events. During infection, ACD2 may bind to and/or reduce PCD-inducing porphyrin-related molecules in mitochondria and possibly chloroplasts that generate reactive oxygen species, cause altered organelle behavior, and activate a cascade of PCD-inducing events.     

A programmed cell death pathway activated in carrot cells cultured at low cell density

Programmed cell death (PCD) occurs in plants during development and defense, but the processes and mechanisms are not yet defined. Culture of carrot single cells at a cell density of <10⁴ cells ml⁻¹ activates a cell death process involving condensation and shrinkage of the cytoplasm and nucleus and fragmentation of the DNA. Modest abiotic stress treatments also cause cell condensation and shrinkage and the formation of DNA fragments, but the same abiotic stresses at high levels cause rapid necrosis with cell swelling and lysis. The common morphological features of cells dying at low cell density and following modest abiotic stress treatments suggest that these features reveal a PCD pathway in carrot. The addition of a cell-conditioned growth medium allows cells at low cell density to remain alive, demonstrating that cell-derived signal molecules suppress a pathway that is otherwise induced by default. Differences in the morphology of the dead cells suggest that proteolysis during PCD differs in detail in plants and animals; however, these findings show that plants, like animals, can control PCD by social signaling, and imply that the mechanism of PCD in plants and animals may be similar. Consistent with this, manipulation of signal pathway intermediates that regulate PCD in animals shows that Ca²⁺ and protein phosphorylation events are PCD pathway intermediates in carrot.     

Nitric oxide acts as an antioxidant and delays programmed cell death in barley aleurone layers

Nitric oxide (NO) is a freely diffusible, gaseous free radical and an important signaling molecule in animals. In plants, NO influences aspects of growth and development, and can affect plant responses to stress. In some cases, the effects of NO are the result of its interaction with reactive oxygen species (ROS). These interactions can be cytotoxic or protective. Because gibberellin (GA)-induced programmed cell death (PCD) in barley (Hordeum vulgare cv Himalaya) aleurone layers is mediated by ROS, we examined the effects of NO donors on PCD and ROS-metabolizing enzymes in this system. NO donors delay PCD in layers treated with GA, but do not inhibit metabolism in general, or the GA-induced synthesis and secretion of alpha-amylase. alpha-Amylase secretion is stimulated slightly by NO donors. The effects of NO donors are specific for NO, because they can be blocked completely by the NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide. The antioxidant butylated hydroxy toluene also slowed PCD, and these data support our hypothesis that NO is a protective antioxidant in aleurone cells. The amounts of CAT and SOD, two enzymes that metabolize ROS, are greatly reduced in aleurone layers treated with GA. Treatment with GA in the presence of NO donors delays the loss of CAT and SOD. We speculate that NO may be an endogenous modulator of PCD in barley aleurone cells.     

Al3+对大豆根边缘细胞程序性死亡诱导的生理生态作用

 设置不同的Al ³⁺浓度（0、25、50、100、200、400 μmol·L^-1）和培养时间 （12、24 h）,研究了边缘细胞活性和大豆（Glycine max）根中 过氧化氢酶（CAT）、过氧化物酶POD）、超氧化物歧化酶SOD）随Al ³⁺浓度及处理时间变化的规律,并通过Hoec hst333 42-PI双重荧光染色、 梯状DNA（即DNA ladder）分析和末端脱氧核糖核酸转移酶介导的dUTP切口末端标记（即TUNEL原位标记）检测,研究了Al ³⁺对大豆根边缘细胞 程序性死亡诱导的生理生态作用。结果表明,Al ³⁺胁迫能诱导边缘细胞的死亡,随着Al ³⁺浓度的升高和处理时间的延长,细胞死亡率增加。通 过Hoechst33342-PI双重荧光染色、DNA ladder分析和TUNEL原位标记,检测到Al ³⁺胁迫下发生程序性死亡的边缘细胞。其表现为：在 400μmol·L^-1 Al ³⁺诱导大豆根24 h时, 核酸电泳显示细胞DNA发生特异性降解并形成阶梯状电泳条带(DNA ladder),用TUNEL原位标记检测200 和400μmol·L^-1 Al ³⁺处理12 h后的大豆根 边缘细胞,发现DNA的3′-OH端被原位特异标记,二氨基联苯胺（DAB）显色后,细胞核为阳性或强 阳性。同时,高浓度Al ³⁺ （＞100μmol·L^-1）处理下,CAT、POD和S OD活性均有不同程度的下降,CAT和SOD的活性也随处理时间的延长而降低 。说明在Al ³⁺胁迫下边缘细胞的死亡可能是一种程序性死亡形式,高浓度Al ³⁺胁迫下,通过诱导活性氧在细胞体内的产生和累积而导致细胞凋 亡,此过程是其对逆境胁迫所作出的生理生态防御性应答方式之一。     

植物中的细胞程序性死亡

细胞程序性死亡（ＰＣＤ）对于维持植物的正常生长发育非常重要,目前已成为植物学研究的一个热点。本文综合评述了近年来植物ＰＣＤ研究的某些进展,包括植物ＰＣＤ的特征,植物的营养生长、生殖生长以及与环境互作过程中存在的各种ＰＣＤ及其证据,植物ＰＣＤ发生的分子机制及其调控等等。对植物ＰＣＤ研究中有待进一步解决的问题和可能意义提出了自己的见解。