多胺参与细胞程序性死亡调控的研究进展

多胺被认为是影响细胞存活的一个关键分子。有证据显示,多胺可直接或间接参与细胞程序性死亡的调控。多胺与细胞程序性死亡直接相关,是指其参与特定的生物学过程及与导致细胞程序性死亡的分子/结构发生相互作用;间接相关,是指多胺通过调控细胞程序性死亡的代谢衍生物,如异化和互变产物来调控这一过程。此外,多胺代谢过程中的细胞毒性产物也参与到细胞程序性死亡的级联反应中。因此,对动植物中依赖于多胺的细胞程序性死亡的最新研究进展进行综述,可为进一步研究提供一些参考。     

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。     

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。     

细胞程序性死亡通路的研究进展

细胞程序性死亡(programmed cell death,PCD)一直被看做是细胞凋亡(apoptosis).随着细胞生物学研究的深入,新的细胞死亡途径逐渐被揭示出来,如胀亡、自噬、副凋亡等.这些通路有些是caspase依赖的,有些不依赖于caspase途径.在细胞程序性死亡过程中,各种通路不是单独起作用的,而是相互交联的,有彼此重叠的机制出现.目前,Clarke形态学分类法是得到大多数学者认可的细胞程序性死亡的分类方式.按照该分类法,可将PCD分为3大类,即:Ⅰ型细胞程序性死亡、Ⅱ型细胞程序性死亡和Ⅲ型细胞程序性死亡.     

胱冬肽酶非依赖性的细胞程序性死亡

在多细胞有机体的组织内稳态维持和正常发育过程中,细胞程序性死亡发挥着重要的作用。细胞程序性死亡有多种形式(如细胞凋亡、类细胞凋亡和类坏死等),其中了解较清楚的是细胞凋亡。一直以来,胱冬肽酶(caspase)被认为是细胞凋亡发生中关键的一种蛋白酶。但是最近的研究表明,包括细胞凋亡在内的一些细胞程序性死亡可以以一种不依赖胱冬肽酶的方式发生。细胞程序性死亡与胱冬肽酶之间存在非依赖性关系。     

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。     

硝基苯对蚕豆根尖细胞凋亡的影响

细胞凋亡(apoptosis)是一自然生理过程。是由一个主动由基因决定的自动结束生命的过程。由于细胞凋亡受到严格的由遗传机制决定的程序性调控,所以也常常被称为细胞程序性死亡(PCD,programmed cell death)。植物在正常发育时也会发生细胞程序性死亡,     

mazEF系统介导胁迫诱导细菌细胞程序性死亡

mazEF是细菌染色体上的“毒素?抗毒素系统”基因(Toxin-antitoxin system, TA系统), 可介导胁迫诱导细菌细胞程序性死亡。本文介绍了mazEF系统的遗传结构特征、生理生化功能、环境胁迫激活mazEF系统介导的细菌细胞程序性死亡的机制, 参与细胞死亡过程中的细胞信号和细胞因子的调控, 以及关于mazEF系统介导的细菌细胞程序性死亡理论的争论, 提出了进一步丰富和完善细菌细胞程序性死亡理论亟待解决的问题。     

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。     

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.     

How an organism dies affects the fitness of its neighbors

Programmed cell death (PCD), a genetically regulated cell suicide program, is ubiquitous in the living world. In contrast to multicellular organisms, in which cells cooperate for the good of the organism, in unicells the cell is the organism and PCD presents a fundamental evolutionary problem. Why should an organism actively kill itself as opposed to dying in a nonprogrammed way? Proposed arguments vary from PCD in unicells being maladaptive to the assumption that it is an extreme form of altruism. To test whether PCD could be beneficial to nearby cells, we induced programmed and nonprogrammed death in the unicellular green alga Chlamydomonas reinhardtii. Cellular contents liberated during non-PCD are detrimental to others, while the contents released during PCD are beneficial. The number of cells in growing cultures was used to measure fitness. Thermostability studies revealed that the beneficial effect of the PCD supernatant most likely involves simple heat-stable biomolecules. Non-PCD supernatant contains heat-sensitive molecules like cellular proteases and chlorophyll. These data indicate that the mode of death affects the origin and maintenance of PCD. The way in which an organism dies can have beneficial or deleterious effects on the fitness of its neighbors.     

Programmed death in a unicellular organism has species-specific fitness effects

Programmed cell death (PCD) is an ancient phenomenon and its origin and maintenance in unicellular life is unclear. We report that programmed death provides differential fitness effects that are species specific in the model organism Chlamydomonas reinhardtii. Remarkably, PCD in this organism not only benefits others of the same species, but also has an inhibitory effect on the growth of other species. These data reveal that the fitness effects of PCD can depend upon genetic relatedness.     

Systems biology of yeast cell death

Programmed cell death (PCD) (including apoptosis) is an essential process, and many human diseases of high prevalence such as neurodegenerative diseases and cancer are associated with deregulations in the cell death pathways. Yeast Saccharomyces cerevisiae, a unicellular eukaryotic organism, shares with multicellular organisms (including humans) key components and regulators of the PCD machinery. In this article, we review the current state of knowledge about cell death networks, including the modeling approaches and experimental strategies commonly used to study yeast cell death. We argue that the systems biology approach will bring valuable contributions to our understanding of regulations and mechanisms of the complex cell death pathways.     

Accelerated cell death in Podospora autophagy mutants

Although autophagy is characteristic of type II programmed cell death (PCD), its role in cell death is currently debated. Both cell death-promoting and prosurvival roles of autophagy have been reported depending on the organism and the cell type. In filamentous fungi, a cell death reaction known as an incompatibility reaction occurs when cells of unlike genotype fuse. Cell death by incompatibility is characterized by a dramatic vacuolar enlargement and cell lysis. In Podospora anserina, autophagy is induced early during this cell death reaction. Cell death by incompatibility in Podospora is a model of type II PCD used here to assess the role of autophagy in this type of cell death. We have inactivated PaATG1, the Podospora ortholog of the Saccharomyces cerevisiae ATG1 gene involved in the early steps of autophagy in yeast. The DeltaPaATG1 mutant displays developmental defects characteristic of abrogated autophagy in Podospora. Using the green fluorescent protein-PaATG8 autophagosome marker, we show that autophagy is abolished in this mutant. Neither cell death by incompatibility nor vacuolization are suppressed in DeltaPaATG1 and DeltaPaATG8 autophagy mutants, indicating that a vacuolar cell death reaction without autophagy occurs in Podospora. Our results thus provide a novel example of a type II PCD reaction in which autophagy is not the cause of cell death. In addition, we found that cell death is accelerated in DeltaPaATG null mutants, suggesting that autophagy has a protective role in this type II PCD reaction.     

Programmed cell death: similarities and differences in animals and plants. A flower paradigm

Summary. After an overview of the criteria for the definition of cell death in the animal cell and of its different types of death, a comparative analysis of PCD in the plant cell is reported. The cytological characteristics of the plant cell undergoing PCD are described. The role of plant hormones and growth factors in the regulation of this event is discussed with particular emphasis on PCD activation or prevention by polyamine treatment (doses, timing and developmental stage of the organism) in a Developmental cell death plant model: the Nicotiana tabacum (tobacco) flower corolla. Some of the effects of polyamines might be mediated by transglutaminase catalysis. The activity of this enzyme was examined in different parts of the corolla during its life span showing an acropetal trend parallel to the cell death wave. The location of transglutaminase in some sub-cellular compartments suggests that it exerts different functions in the corolla DCD.     

The lace plant: a novel model system to study plant proteases during developmental programmed cell death in vivo

Programmed cell death (PCD) plays a major role in plant development and defense throughout the plant kingdom. Within animal systems, it is well accepted that caspases play a major role in the PCD process, although no true caspases have yet to be identified in plants. Despite this, vast amounts of evidence suggest the existence of caspase-like proteases in plants. The lace plant (Aponogeton madagascariensis) forms perforations in a predictable pattern between longitudinal and transverse veins over its entire leaf surface via PCD. Due to the thin nature of the leaf, allowing for long-term live cell imaging, a perfected method for sterile culture, as well as the feasibility of pharmacological experiments, the lace plant provides an excellent model to study developmental PCD. In this review, we report the suitability of the lace plant as a novel organism to study proteases in vivo during developmentally regulated cell death.     

PCD and autophagy in the unicellular green alga Micrasterias denticulata

Programmed cell death (PCD) plays a central role in normal plant development and is also induced by various biotic and abiotic stress factors. In the unicellular freshwater green alga Micrasterias denticulata morphological and biochemical hallmarks such as the appearance of autophagosomes, increased production of ROS and degradation of genomic DNA into small fragments (“DNA laddering”) indicate PCD. Our data not only demonstrate that Micrasterias is capable of performing PCD under salt stress, but also that it is triggered by the ionic and not osmotic component of salinity. Additionally, results from the present and previous studies suggest that different inducers may lead to different cell death pathways in one and the same organism.     

Mechanical insights into the regulation of programmed cell death by p53 via mitochondria

All organisms end with their death, and many parts of cells die through intrinsic suicide machineries in response to diverse stimuli. These intrinsic cell death pathways are often termed as programmed cell deaths (PCDs), and are critical for organism development, tissue homeostasis and various diseases. Recent evidence has revealed that most of PCDs involve a tumor suppressor p53 and components of the intra-mitochondria. Furthermore, the movement and positioning of p53 in cells affect the induction of each PCD pathway. Here we provide a comprehensive review on p53-related PCD mechanisms via the mitochondria, namely classical apoptosis, non-classical apoptosis, autophagic cell death, ferroptosis, necroptosis. In addition, we discuss the roles of p53 in each PCD pathway by focusing its altered intracellular localization in response to diverse cellular stresses.     

Quantum algorithm for programmed cell death of Caenorhabditis elegans

During the development of Caenorhabditis elegans, through cell divisions, a total of exactly 1090 cells are generated, 131 of which undergo programmed cell death (PCD) to result in an adult organism comprising 959 cells. Of those 131, exactly 113 undergo PCD during embryogenesis, subdivided across the cell lineages in the following fashion: 98 for AB lineage; 14 for MS lineage; and 1 for C lineage. Is there a law underlying these numbers, and if there is, what could it be? Here we wish to show that the count of the cells undergoing PCD complies with the cipher laws related to the algorithms of Shor and of Grover.