植物发育过程中的细胞程序性死亡

细胞程序性死亡(PCD)是植物发育过程中必不可少的一部分,近年来对植物发育过程中的细胞程序性死亡机制的研究已经广泛开展。植物发育过程中的PCD对植物自身形态建成和组织分化有重要意义。一般认为动、植物的PCD有很大的相似性,但植物发育过程也有着独特的PCD机制,例如依靠有裂解功能的液泡来参与PCD。通过比较植物和其他生物发育过程中的PCD,可对植物发育过程中PCD的特征有着更深入的了解。说明植物发育过程中PCD的研究将在理论和生产上有重大意义。     

植物细胞程序性死亡的研究进展

细胞程序性死亡（PCD）是生物进化过程中受自身基因控制并受多种因子调控的一种细胞主动的死亡过程。PCD在植物的正常生长发育、对环境胁迫的反应和病原体入侵引发的过敏反应中起重要的作用。简要综述了植物PCD的特征、与此相关的蛋白和活性氧在PCD过程中的作用。     

植物细胞程序化死亡研究进展

细胞程序化死亡 (PCD)是一种由基因控制的、主动的细胞死亡过程 ,它在植物正常生长发育过程中起着重要作用。本文就植物PCD的近期研究进展和其分子信号调控机制作一综合阐述     

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。     

植物细胞程序死亡的机理及其与发育的关系

细胞程序死亡（PCD）是在植物体发育过程中普遍存在的,在发育的特定阶段发生的自然的细胞死亡过程,这一死亡过程是由某些特定基因编码的“死亡程序”控制的。PCD是细胞分化的最后阶段。细胞分化的临界期就处于死亡程序执行中的某个阶段。PCD包含启动期、效应期和清除期三个阶段,其间caspase家族起着重要作用。PCD在细胞和组织的平衡、特化,以及组织分化、器官建成和对病原体的反应等植物发育过程中起着重要作用。PCD中的形态学变化和生物化学变化都有着严格的时序性。植物的PCD和动物的PCD有许多共性,包括细胞形态和DNA降解等变化。也有一些不同,植物PCD的产物既可被其它细胞吸收利用;也可用于构建自身的次生细胞壁。     

植物细胞程序性死亡检测技术研究进展

细胞程序性死亡(PCD)是一种细胞生物学反应,广泛存在于植物的生长发育与抗逆过程,是当今生命科学的研究热点之一。从形态学、生物化学和分子生物学等方面综合分析了植物细胞PCD检测方法的研究进展,并对现有植物PCD检测技术的不足和解决途径进行了讨论与展望,以期为后续PCD研究和应用提供借鉴。     

植物细胞程序性死亡(PCD)的研究进展

细胞死亡是动、植物生长发育过程中常见的一种生命现象 ,而细胞程序性死亡 (PCD)是细胞遵循自身生命活动程序 ,并受多种因子调控的一种积极的死亡方式。近年来随着动物中PCD研究的深入 ,植物PCD亦得到相应的研究。植物细胞程序性死亡研究不仅可揭示植物衰老、死亡的内部变化规律 ,而且可为其生长发育的调控提供依据和技术。该文试对有关PCD的特点、研究意义及近年来的研究概况与方法进行简述与评价。     

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。     

植物Metacaspase研究进展

过敏性坏死反应是植物的一种重要的抗病机制, 类似于动物细胞凋亡, 它是一种程序性细胞死亡(programmed cell death, PCD)过程。目前, 已经确定半胱天冬蛋白酶(caspase)在动物PCD过程中起核心作用。在植物中, 尚未发现其直系同源蛋白, 但是有一类与其结构相似的蛋白酶, 称为metacaspase。在植物不同的PCD过程中, 有的依赖于metacaspase, 而有的则不依赖于该类蛋白酶。目前对metacaspase的结构和功能已有了初步的研究, 对其深入的研究则进展缓慢, 其具体的生物学功能和在PCD信号路径中的定位有待进一步探索。     

FRET技术检测植物类caspase-3蛋白酶活性的质粒构建及其瞬时表达

植物细胞程序性死亡（programmed cell death,PCD）是一种由细胞内部程序控制的、主动的细胞死亡过程。在植物发育、逆境胁迫及超敏反应中,PCD都起着重要的作用。为检测植物PCD过程中类似动物细胞凋亡蛋白酶caspase-3的活性,构建了一个能够在活体植物细胞中实时检测类caspase-3蛋白酶激活的质粒PI—ECFP—EYFP。该质粒在植物细胞中可以表达出两端为青色荧光蛋白（ECFP）和黄色荧光蛋白（EYFP）的融合蛋白。这两个荧光蛋白通过含有caspase-3蛋白酶作用靶点DEVD的短肽相连,从而可以根据荧光共振能量转移现象检测类caspase-3凋亡蛋白酶的激活,以为实时检测植物PCD过程中关键蛋白酶的激活及其调控奠定基础。     

Salt stress induces programmed cell death in prokaryotic organism Anabaena

AIMS: Our main interest is to check if programmed cell death (PCD) can occur in prokaryotic algae and if the morphological and biochemical features of PCD are conserved. METHODS AND RESULTS: Using TUNEL labelling, fluorescence and light microscopy and DNA gel electrophoresis, we found that cell death with features similar to those in metazoan PCD could be induced in different Anabaena strains after exposure to univalent-cation salts at moderate concentration. These features included specific DNA fragmentation, cytoplasmic vacuolation, and the progressive disorganization, fragmentation and subsequent autolysis of the cell corpse. Further analyses of cell viability and proteinase activity revealed that increased protease activities, decreased DNA content, and loss of plasmalemma integrity were related to the PCD process. CONCLUSIONS: The results showed that like PCD in eukaryotes, PCD in Anabaena is an active process, and is an adaptation to adverse environments. The features of PCD shared between eukaryotes and Anabaena suggest that PCD mechanisms are conserved during evolution. SIGNIFICANCE AND IMPACT OF THE STUDY: The results will contribute greatly to our understanding of PCD origin and evolution, and are potentially useful in controlling the deluge of algae in some lakes.     

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.     

Autophagy regulates programmed cell death during the plant innate immune response

The plant innate immune response includes the hypersensitive response (HR), a form of programmed cell death (PCD). PCD must be restricted to infection sites to prevent the HR from playing a pathologic rather than protective role. Here we show that plant BECLIN 1, an ortholog of the yeast and mammalian autophagy gene ATG6/VPS30/beclin 1, functions to restrict HR PCD to infection sites. Initiation of HR PCD is normal in BECLIN 1-deficient plants, but remarkably, healthy uninfected tissue adjacent to HR lesions and leaves distal to the inoculated leaf undergo unrestricted PCD. In the HR PCD response, autophagy is induced in both pathogen-infected cells and distal uninfected cells; this is reduced in BECLIN 1-deficient plants. The restriction of HR PCD also requires orthologs of other autophagy-related genes including PI3K/VPS34, ATG3, and ATG7. Thus, the evolutionarily conserved autophagy pathway plays an essential role in plant innate immunity and negatively regulates PCD.     

Paradoxical roles for programmed cell death signaling during viral infection of the central nervous system

Programmed cell death (PCD) is an essential mechanism of antimicrobial defense. Recent work has revealed an unexpected diversity in the types of PCD elicited during infection, as well as defined unique roles for different PCD modalities in shaping the immune response. Here, we review recent work describing unique ways in which PCD signaling operates within the infected central nervous system (CNS). These studies reveal striking complexity in the regulation of PCD signaling by CNS cells, including both protective and pathological outcomes in the control of infection. Studies defining the specialized molecular mechanisms shaping PCD responses in the CNS promise to yield much needed new insights into the pathogenesis of neuroinvasive viral infection, informing future therapeutic development.     

PANoptosis in Viral Infection: The Missing Puzzle Piece in the Cell Death Field

In the past decade, emerging viral outbreaks like SARS-CoV-2, Zika and Ebola have presented major challenges to the global health system. Viruses are unique pathogens in that they fully rely on the host cell to complete their lifecycle and potentiate disease. Therefore, programmed cell death (PCD), a key component of the host innate immune response, is an effective strategy for the host cell to curb viral spread. The most well-established PCD pathways, pyroptosis, apoptosis and necroptosis, can be activated in response to viruses. Recently, extensive crosstalk between PCD pathways has been identified, and there is evidence that molecules from all three PCD pathways can be activated during virus infection. These findings have led to the emergence of the concept of PANoptosis, defined as an inflammatory PCD pathway regulated by the PANoptosome complex with key features of pyroptosis, apoptosis, and/or necroptosis that cannot be accounted for by any of these three PCD pathways alone. While PCD is important to eliminate infected cells, many viruses are equipped to hijack host PCD pathways to benefit their own propagation and subvert host defense, and PCD can also lead to the production of inflammatory cytokines and inflammation. Therefore, PANoptosis induced by viral infection contributes to either host defense or viral pathogenesis in context-specific ways. In this review, we will discuss the multi-faceted roles of PCD pathways in controlling viral infections.     

Programmed cell death in trypanosomatids: a way to maximize their biological fitness?

Programmed cell death (PCD) is a biochemical process that plays an essential role in the development of multicellular organisms. However, accumulating evidence indicates that PCD is also present in single-celled eukaryotes. Thus, trypanosomatids might be endowed with a PCD mechanism that is derived from ancestral death machinery. PCD in trypanosomatids could be a process without a defined function, inherited through eukaryotic cell evolution, which might be triggered in response to diverse stimuli and stress conditions. However, recent observations suggest that PCD might be used by trypanosomatids to maximize their biological fitness. Therefore, PCD could represent a potential pharmacological target for protozoan control.     

The involvement of cysteine proteases and protease inhibitor genes in the regulation of programmed cell death in plants

Programmed cell death (PCD) is a process by which cells in many organisms die. The basic morphological and biochemical features of PCD are conserved between the animal and plant kingdoms. Cysteine proteases have emerged as key enzymes in the regulation of animal PCD. Here, we show that in soybean cells, PCD-activating oxidative stress induced a set of cysteine proteases. The activation of one or more of the cysteine proteases was instrumental in the PCD of soybean cells. Inhibition of the cysteine proteases by ectopic expression of cystatin, an endogenous cysteine protease inhibitor gene, inhibited induced cysteine protease activity and blocked PCD triggered either by an avirulent strain of Pseudomonas syringae pv glycinea or directly by oxidative stress. Similar expression of serine protease inhibitors was ineffective. A glutathione S-transferase-cystatin fusion protein was used to purify and characterize the induced proteases. Taken together, our results suggest that plant PCD can be regulated by activity poised between the cysteine proteases and the cysteine protease inhibitors. We also propose a new role for proteinase inhibitor genes as modulators of PCD in plants.     

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.     

Promoter analysis of the Drosophila melanogaster gene encoding the pterin 4alpha-carbinolamine dehydratase.

Pterin-4alpha-carbinolamine dehydratase (PCD) is a key enzyme in the regeneration pathway of tetrahydrobiopterin. Previously, we isolated and reported the Drosophila melanogaster gene encoding PCD. In the present study, we isolated and characterized the Drosophila virilis gene encoding PCD. The Drosophila virilis PCD gene has two introns and an open reading frame to encode a protein of 101 amino acids. The amino acid sequence of Drosophila virilis PCD shows a 83% homology to that of the Drosophila melanogaster PCD protein. From the alignment of the nucleotide sequence in the 5'-flanking region of the Drosophila melanogaster and Drosophila virilis PCD genes, we found four conserved sequences. Using a transient transfection assay, we showed that one of the conserved sequences (-127 to approximately -115) is critical for expression, also the minimal promoter region between -127 and +51 is necessary for the efficient expression of Drosophila melanogaster PCD.