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1.
Controlled cellular suicide is an important process that can be observed in various organs during plant development. From the generation of proper sexual organs in monoecious plants to the hypersensitive response (HR) that occurs during incompatible pathogen interactions, programmed cell death (PCD) can be readily observed. Although several biochemical and morphological parameters have been described for various types of cell death in plants, the relationships existing between those different types of PCD events remain unclear. In this work, we set out to examine if two early molecular markers of HR cell death (HIN1 and HSR203J) as well as a senescence marker (SAG12) are coordinately induced during these processes. Our result indicates that although there is evidence of some cross-talk between both cell death pathways, spatial and temporal characteristics of activation for these markers during hypersensitive response and senescence are distinct. These observations indicate that these markers are relatively specific for different cell death programs. Interestingly, they also revealed that a senescence-like process seems to be triggered at the periphery of the HR necrotic lesion. This suggests that cells committed to die during the HR might release a signal able to induce senescence in the neighboring cells. This phenomenon could correspond to the establishment of a second barrier against pathogens. Lastly, we used those cell death markers to better characterize cell death induced by copper and we showed that this abiotic induced cell death presents similarities with HR cell death.  相似文献   

2.
  总被引:4,自引:0,他引:4  
Activation of the tobacco gene hsr203 is rapid, highly localized, specific for incompatible plant-pathogen interactions, and strongly correlated with programmed cell death occurring in response to diverse pathogens. Functional characterization of hsr203 gene product has shown that HSR203 is a serine hydrolase that displays esterase activity. We show here that transgenic tobacco plants deficient in HSR203 protein exhibit an accelerated hypersensitive response when inoculated with an avirulent strain of Ralstonia solanacearum. This response was accompanied by a maximal level of cell death and a drastic inhibition of in planta bacterial growth. Transgenic plants deficient in HSR203 were also found to show increased resistance in a dosage-dependent manner to Pseudomonas syringae pv. pisi, another avirulent bacterial pathogen, and to virulent and avirulent races of Phytophthora parasitica, a fungal pathogen of tobacco, but not to different virulent bacteria. Surprisingly, expression of another hsr gene, hsr515, and that of the defence genes PR1-a and PR5, was strongly reduced in the transgenic lines. Our results suggest that hsr203 antisense suppression in tobacco can have pleiotropic effects on HR cell death and defence mechanisms, and induces increased resistance to different pathogens.  相似文献   

3.
    
As much as the definition of life may be controversial, the definition of death also may prove problematic. In recent years it became apparent that the death of a living cell may follow more than one possible scenario: it may result from an externally applied physical injury (an accidental death), or it may be the outcome of activating an internal pathway for cell suicide (a programmed death). That cells can participate in their own execution may indicate that certain types of cell deaths that were previously considered to be caused by foreign agents such as pathogens or drugs may actually result from the activation of a programmed cell death pathway that is normally latent in cells. Here, we describe the activation of such a cell suicide pathway in plant cells upon the recognition of an invading pathogen. We discuss the possible use of this pathway as a defense mechanism against infection and the possibility that in many ways the use of this type of cell death in plants is functionally analogous to that used by mammalian cells in response to infection by pathogens. Dev. Genet. 21:279–289, 1997. © 1997 Wiley-Liss, Inc.  相似文献   

4.
Mittler  Ron  Lam  Eric 《Plant molecular biology》1997,34(2):209-221
Programmed cell death (PCD) is activated during the response of multicellular organisms to some invading pathogens. One of the key aspects of this process is the degradation of nuclear DNA which is thought to facilitate the recycling of DNA from dead cells. The PCD of tobacco plants (genotype NN) infected with tobacco mosaic virus (TMV) is accompanied by the induction of nuclease activities and the cleavage of nuclear DNA to fragments of about 50 kb. We examined the correlation between the increase in nuclease activities and the fragmentation of nuclear DNA during TMV- and bacteria-induced PCD in tobacco. We found that the increase in nuclease activities did not always correlate with fragmentation of nuclear DNA. Thus, in addition to pathogens that induce PCD, mechanical injury and infiltration of leaves with 1 M sucrose or bacteria that did not induce PCD also resulted in an increase in nuclease activities. Analysis of nuclease activities in total leaf extracts, nuclear extracts, and intercellular fluid (i.e., apoplast) revealed that at least four different nuclease activities are induced during PCD in tobacco; of these at least three appear to be secreted into the intercellular fluid. Although the latter were also induced in response to treatments that did not result in DNA fragmentation, they may function in the recycling of plant DNA during late stages of PCD when the integrity of the plasma membrane is compromised. This suggestion is supported by the finding that DNA degradation occurred late during TMV-induced PCD in tobacco. In addition, the finding of induced nuclease activities in the intercellular fluid raises the possibility that they may serve a protective function by degrading the DNA of invading pathogens.  相似文献   

5.
李磊  贡豪  李韬 《生物技术进展》2018,8(6):509-516
很多植物通过过敏反应产生广谱抗病性,类过敏反应发生机制的解析以及相关基因的研究对培育广谱抗病品种、提高作物的适应性和稳产性具有重要意义。植物类过敏反应介导的抗病性可大致分为活性氧迸发、信号分子的传递以及抗病系统的激活三个阶段,对这三个阶段的最新研究进展进行了综述,以期为植物抗病相关研究提供参考。  相似文献   

6.
Studies on plant–pathogen interactions often involve monitoring disease symptoms or responses of the host plant to pathogen-derived immunogenic patterns, either visually or by staining the plant tissue. Both these methods have limitations with respect to resolution, reproducibility, and the ability to quantify the results. In this study we show that red light detection by the red fluorescent protein (RFP) channel of a multipurpose fluorescence imaging system that is probably available in many laboratories can be used to visualize plant tissue undergoing cell death. Red light emission is the result of chlorophyll fluorescence on thylakoid membrane disassembly during the development of a programmed cell death process. The activation of programmed cell death can occur during either a hypersensitive response to a biotrophic pathogen or an apoptotic cell death triggered by a necrotrophic pathogen. Quantifying the intensity of the red light signal enables the magnitude of programmed cell death to be evaluated and provides a readout of the plant immune response in a faster, safer, and nondestructive manner when compared to previously developed chemical staining methodologies. This application can be implemented to screen for differences in symptom severity in plant–pathogen interactions, and to visualize and quantify in a more sensitive and objective manner the intensity of the plant response on perception of a given immunological pattern. We illustrate the utility and versatility of the method using diverse immunogenic patterns and pathogens.  相似文献   

7.
8.
A previous study had indicated that scavengers of reactive oxygen species (ROS) delayed cell death (the hypersensitive response (HR)) triggered in epidermal cells of intact, resistant, cowpea ( Vigna unguiculata (L.) Walp) leaves by the monokaryotic stage of the cowpea rust fungus ( Uromyces vignae Barclay race 1). This HR had been monitored by cell autofluorescence, which occurs after protoplast collapse. In the present study, when cytoplasmic disorganization was used to monitor cell death more directly, ROS-scavengers, superoxide dismutase, catalase, horseradish peroxidase, and desferal-Mn(IV) had no effect on HR development. Cytological staining for superoxide or hydrogen peroxide generation also did not reveal the presence of ROS before or during the early stages of the HR, but did, as in the previous study, suggest a role in the autofluorescence and browning of invaded cells that occur following protoplast collapse. Staining of plant mitochondria with nitroblue tetrazolium, possibly attributable to increased dehydrogenase activity but not superoxide generation, occurred transiently around invasion hyphae (monokaryotic stage of the fungus) or haustoria (dikaryotic stage) of the fungus as they entered a cell in the susceptible or resistant cultivar. Around invasion hyphae in epidermal cells in resistant plants, this staining diminished as cytoplasmic streaming stopped, and gradually disappeared as cell death progressed. These data are consistent with other evidence that rust fungi initially negate non-specific defensive responses in both resistant and susceptible cells as part of the establishment of biotrophy. They also suggest that the HR in the cowpea–cowpea rust fungus pathosystem is not triggered by an oxidative burst.  相似文献   

9.
10.
The emergence of the adult Manduca sexta moth is accompained by the death of half of the neurons present in the pupal abdominal nervous system (Truman, 1983). This developmental neuronal death is highly selective, so that the same neurons die at the same time relative to emergence in every moth. In the case of the MN-12 motoneurons, this cell death is regulated both by hemolymph concentrations of a steroid hormone, 20-hydroxyecdysone, and by actions exerted by adjacent ganglia (Truman and Schwartz, 1984; Fahrbach and Truman, 1987). This latter effect, which has been previously described in isolated abdomens and in moths with transected ventral nerve cords, has now been reproduced under controlled culture conditions in which the selectivity and extent of postemergence neuronal death is comparable to that seen in vivo. With respect to the MN-12 neurons found in the most anterior unfused abdominal ganglion, A3, the pterothoracic ganglion appears to be the source of a factor that permits these neurons to die according to their usual developmental schedule. © 1992 John Wiley & Sons, Inc.  相似文献   

11.
镉诱导的茶树苗膜脂过氧化和细胞程序性死亡   总被引:28,自引:1,他引:28  
在含镉的营养液中,茶树幼苗生长受到抑制。随培养时间延长,膜脂过氧化产物丙二醛含量持续升高;超氧物岐化酶(SOD)和过氧化氢酶(CAT)活性初期升高,而后分别在第4天和第2天开始下降。镉胁迫的第5-7天,一部分细胞陆续发生程序性死亡。其特征是:线粒体聚集于核周围,个数增加,嵴发达,而后衰亡。核仁消失,染色质凝结在核膜边缘,核萎缩,外层核膜局部扩张,形成胀泡。核以外溢、出芽和崩裂三种方式溃解。核是最后消亡的细胞器。程序性死亡的细胞局限于某些区域。镉胁迫下,幼苗膜脂过氧化可能是诱发PCD的主要原因。  相似文献   

12.
以烟草和拟南芥中的单拷贝抗病基因myb1和NDR1作探针,利用荧光原位杂交的方法分别对这两个基因在玉米(Zea mays L.)和烟草(Nicotiana tabacum L.)、玉米和拟南芥(Arabidopsis thaliana(L.)Heynh.)中的同源性做了研究。杂交结果表明myb1和NDR1的同源序列分别位于玉米第8、5染色体,单个信号位置表明0这两个基因的同源序列在玉米基因组中只有  相似文献   

13.
Regulators of cell death in disease resistance   总被引:17,自引:0,他引:17  
Cell death and disease resistance are intimately connected in plants. Plant disease resistance genes (R genes) are key components in pathogen perception and have a potential to activate cell death pathways. Analysis of R proteins suggests common molecular mechanisms for pathogen recognition and signal emission whereas the subsequent signalling unexpectedly involves a network of pathways of parallel, branching and converging action. Disease resistance signalling mutants have revealed novel types of regulatory proteins whose biochemical functions are still unknown. Accumulation of small molecules such as salicylic acid, reactive oxygen intermediates, and nitric oxide amplifies resistance responses and directs cells to initiate cell death programs. Genetic analyses of lesion mimic mutants provide a glimpse of how cell death thresholds are set via an interplay of positive and negative regulatory components.  相似文献   

14.
    
Using fluorescence in situ hybridization, the authors investigated the homology between three plant species, maize (Zea mays L.) and tobacco (Nicotiana tabacum L.), maize and Arabidopsis thaliana (L.) Heynh. at cytogenetic level using two probes corresponding to functional disease resistance genes myb1 and NDR1 in Arabidopsis and tobacco respectively. The hybridization signals of the tested probes were detected in maize chromosomes 8 and 5 respectively, and the single location of each of the two probes showed only single copy of them in maize genome. The results provided a valuable insight into searching for genes associated with programmed cell death in plants using heterologous probe with comparative genetic approach. In addition, the improvements of FISH technique using heterologous probes were discussed.  相似文献   

15.
Exogenously applied methyl jasmonate (MeJA) might induce the formation of necrotic lesions that closely resemble hypersensitive response lesions. Cellular damage, restricted to the infiltrated zone, was accompanied with the production of H2O2 from the oxidative burst. H2O2 generated in response to MeJA can be histochemically detected in cells surrounding the necrotic lesions as well as in the vascular tissues. The response is systemic and maximizes with time. Among 12 plant species from different families that were assayed for both hypersensitive reaction (HR)-like response and H2O2 generation, only woody species exhibited both MeJA-inducible HR cell death and the generation of H2O2. To assess the role of H2O2 in MeJA-induced HR-like cell death, a gain and loss of function strategy was employed. The cumulative results indicate that H2O2 is neither necessary nor sufficient for MeJA-inducible cell death and that O2 rather than H2O2 might be responsible.  相似文献   

16.
    
One of the earliest signal transduction events that trigger the hypersensitive response (HR) of plants against pathogen attack is thought to be an alteration of proton flux across the plasma membrane (PM). However, no direct genetic evidence for the involvement of PM-localised proton channels or pumps in the induction of this response has been reported. We previously showed that expression of the bacterial proton pump bacterio-opsin (bO) in transgenic plants resulted in the spontaneous activation of the HR. Here we show that the bO protein is likely localised to the PM in transgenic tobacco plants. Furthermore, mutational analysis shows that induction of the HR by bO expression is dependent upon the capability of bO to translocate protons. Although bO functions as a light-driven proton pump in Halobacteria when assembled with retinal, we also show by mutational analysis that this chromophore binding is unnecessary for its in planta activity. Taken together, our results suggest that expression of bO in plants leads to the insertion of a passive proton channel into the PM. The activity of this channel in the PM results in spontaneous activation of cell death and HR-associated phenotypes including enhanced resistance to a broad spectrum of plant pathogens. Our work provides direct molecular evidence to support a working model in which alterations in ionic homeostasis at the level of the PM may work as one of the critical steps in the signalling pathway for the activation of the HR.  相似文献   

17.
18.
Treatment of Taxus chinensis cell suspension cultures with fungal elicitor resulted in an oxidative stress characterized by H2O2 production, malondiadehyde (MDA) accumulation and cell death. This oxidative stress was dependent on the concentration of elicitor. Cells exposed to elicitor accumulated taxol, however, not proportional to elicitor concentration. High production of taxol occurred in cells treated with the suitable elicitor concentration. We concluded that oxidative stress had the deleterious effect on taxol production. Simultaneous treatment with elicitor and ascorbic acid (ASA) changed the oxidative stress and taxol production. Production of taxol in cells treated with 200 mg dm–3 elicitor and ASA was enhanced compared with that in cells treated with only 200 mg dm–3 elicitor, while production of taxol in cells treated with 100 and 50 mg dm–3 elicitor and ASA was decreased compared with that in cells treated with 100 and 50 mg dm–3 elicitor.  相似文献   

19.
    
Half of the neurons in the abdominal nervous system of the moth Manduca sexta die after adult eclosion. Two physiological signals regulate post-eclosion neuronal death in adult moths. The first is endocrine: a decline in blood ecdysteroids is necessary for the death of neurons in the segmental ganglia. The second signal, which is highly specific for a pair of motoneurons found at the posterior midline in each of the three unfused abdominal ganglia, originates in the nervous system. It is transmitted from the fused pterothoracic ganglion to abdominal ganglion A3 via the intersegmental connectives. To characterize the signal of neural origin, we have developed an in vitro bioassay for neuron-killing factors (“neurocidins”). Aqueous extracts of pterothoracic ganglia were prepared and applied to cultured ventral nerve cords. These extracts exhibited concentration-dependent effectiveness in killing motoneurons. The active component of the extract was heat-stable and protease-sensitive. Size fractionation studies suggested that the active component has a molecular mass between 10 and 30 kD. This is the first report of an endogenous neuron-killing protein from an insect nervous system. © 1995 Wiley-Liss, Inc.  相似文献   

20.
  总被引:7,自引:0,他引:7  
Tropospheric ozone will increase during the next decades and will reach the critical threshold concentration of 40 nl l−1 more often in rural regions than in urban areas. Damage inflicted on plants by ozone can be divided into chronic and acute damage, reflecting different defence strategies of the plants. Chronic damage, somewhat similar to a premature senescence, follows disturbances in sugar metabolism, inhibition of photosynthesis, disbalances in the redox-status and ROS-production in the chloroplast stroma. The acute damage resembles the hypersensitive response which occurs after a pathogen attack. Either the accumulation of reactive oxygen species (ROS) or the efficiency of scavenging systems in the apoplast may govern the spread of cell death. Probably, different signalling pathways mediate the plant responses, such as ethylene, salicylate and ROS. ROS production and lipid peroxidation take place either on the plasma membrane or in the chloroplastic membrane and lipid hydroperoxides and derivatives, such as jasmonate, can act as signals for subsequent plant reactions. Both kinds of plant responses, i.e., acute as well as chronic damage, can affect the plants' abilities to respond to further stress attacks.  相似文献   

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