• The Plant Pathology Journal
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• v.21 no.2
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• pp.99-101
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• 2005

Host cell death occurs during many, but not all, interactions between plants and the pathogens that infect them. This cell death can be associated with disease resistance or susceptibility, depending on the nature of the pathogen. The most well-known cell death response in plants is the hypersensitive response (HR) associated with a resistance response. HR is commonly regulated by direct or indirect interactions between avirulence proteins from pathogen and resistance proteins from plant and it can be the result of multiple signaling pathways. Ion fluxes and the generation of reactive oxygen species commonly precede cell death, but a direct involvement of the latter seems to vary with the plant-pathogen combination. Exciting advances have been made in the identification of cellular protective components and cell death suppressors that might operate in HR. In this review, recent progress in the mechanisms by which plant programmed cell death (PCD) occurs during disease resistance will be discussed.

• The Plant Pathology Journal
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• v.15 no.1
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• pp.8-13
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• 1999

Hypersensitive cell death of plants during incompatible plant-pathogen interactions is one of the efficient defense mechanisms of plants against pathogen infections. For better understanding of the molecular mechanisms involved in the plant hypersensitive response (HR), TMV-induced biotic plant cell death and CuSO4-induced abiotic plant cell death were compared in terms of expression patterns of ten different defense-related genes as molecular markers. The genes include five pathogenesis-related protein genes, two plant secondary metabolite-associated genes, two oxidative stress-related genes and one wound-inducible gene isolated from tobacco. Northern blot analyses revealed that a same set of defense-related genes was induced during both biotic and abiotic cell death but with different time and magnitude. The expression of defense-related genes in tobacco plants was temporarily coincided with the time of cell death. However, when suspension cell cultures was used to monitor the expression of defense-related genes, different patterns of the gene expression were detected. This result implies that three are common and, in addition, also different branches of signaling pathways leading to the induced expression of defense-related genes in tobacco during the pathogen- and heavy metal-induced cell death.

• The Plant Pathology Journal
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• v.39 no.6
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• pp.584-591
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• 2023

Active plant immune response involving programmed cell death called the hypersensitive response (HR) is elicited by microbial effectors delivered through the type III secretion system (T3SS). The marine bacterium Hahella chejuensis contains two T3SSs that are similar to those of animal pathogens, but it was able to elicit HR-like cell death in the land plant Nicotiana benthamiana. The cell death was comparable with the transcriptional patterns of H. chejuensis T3SS-1 genes, was mediated by SGT1, a general regulator of plant resistance, and was suppressed by AvrPto1, a type III-secreted effector of a plant pathogen that inhibits HR. Thus, type III-secreted effectors of a marine bacterium are capable of inducing the nonhost HR in a land plant it has never encountered before. This suggests that plants may have evolved to cope with a potential threat posed by alien pathogen effectors. Our work documents an exceptional case of nonhost HR and provides an expanded perspective for studying plant nonhost resistance.

• The Plant Pathology Journal
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• v.40 no.4
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• pp.358-376
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• 2024

Inoculation of Chinese cabbage leaves with high titer (10⁷ cfu/ml) of the non-adapted bacteria Xanthomonas campestris pv. vesicatoria (Xcv) strain Bv5-4a.1 triggered rapid leaf tissue collapses and hypersensitive cell death (HCD) at 24 h. Electrolyte leakage and lipid peroxidation markedly increased in the Xcv-inoculated leaves. Defence-related gene expressions (BrPR1, BrPR4, BrChi1, BrGST1 and BrAPX1) were preferentially activated in the Xcv-inoculated leaves. The Xcv-triggered HCD was attenuated by continuous light but accelerated by a dark environment, and the prolonged high relative humidity also alleviated the HCD. Constant dark and increased relative humidity provided favorable conditions for the Xcv bacterial growth in the leaves. Pretreated fluridone (biosynthetic inhibitor of endogenous abscisic acid [ABA]) increased the HCD in the Xcv-inoculated leaves, but exogenous ABA attenuated the HCD. The pretreated ABA also reduced the Xcv bacterial growth in the leaves. These results highlight that the onset of HCD in Chinese cabbage leaves initiated by non-adapted pathogen Xcv Bv5-4a.1 and in planta bacterial growth was differently modulated by internal and external conditional changes.

• Journal of Plant Biotechnology
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• v.4 no.1
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• pp.1-6
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• 2002

Plants have developed a sophisticated battery of defence responses to protect themselves against attempted pathogen ingress. Manipulation of these defence mechanisms may provide significant opportunities for crop improvement. While plant resistance genes have had a long service history in plant breeding, they possess significant limitations. Recent advances are now providing significant insights into strategies designed to increase the field durability of this class of genes. Hypersensitive cell death is a common feature underlying the deployment of plant defence responses against biographic pathogens. In contrast, necrotrophic pathogens actively kill plant cells. Recently, transgenic plants have been developed that either promote or suppress cell death, providing resistance against either biotrophic or necrotrophic pathogens respectively. Methyl-jasmonate is a key signalling molecule in the establishment of resistance against some fungal pathogens. Increasing the concentration of this molecule in plant cells has been shown to increase resistance against Botrytis cineria, without significantly imparting plant growth or development. Due to the multifarious infection strategies employed by plant pathogens, how-ever, it is unlikely a single commercial product will prove a panacea for global disease control. Future stategies will more likely entail an integrated disease management approach.

• The Plant Pathology Journal
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• v.30 no.3
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• pp.254-260
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• 2014

Potato Rpi-blb2 encodes a protein with a coiled-coil-nucleotide binding site and leucine-rich repeat (CC-NBSLRR) motif that recognizes the Phytophthora infestans AVRblb2 effector and triggers hypersensitive cell death (HCD). To better understand the components required for Rpi-blb2-mediated HCD in plants, we used virus-induced gene silencing to repress candidate genes in Rpi-blb2-transgenic Nicotiana benthamiana plants and assayed the plants for AVRblb2 effector. Rpi-blb2 triggers HCD through NbSGT1-mediated pathways, but not NbEDS1- or NbNDR1-mediated pathways. In addition, the role of salicylic acid (SA), jasmonic acid (JA), and ethylene (ET) in Rpi-blb2-mediated HCD were analyzed by monitoring of the responses of NbICS1-, NbCOI1-, or NbEIN2-silenced or Rpi-blb2::NahG-transgenic plants. Rpi-blb2-mediated HCD in response to AVRblb2 was not associated with SA accumulation. Thus, SA affects Rpi-blb2-mediated resistance against P. infestans, but not Rpi-blb2-mediated HCD in response to AVRblb2. Additionally, JA and ET signaling were not required for Rpi-blb2-mediated HCD in N. benthamiana. Taken together, these findings suggest that NbSGT1 is a unique positive regulator of Rpi-blb2-mediated HCD in response to AVRblb2, but EDS1, NDR1, SA, JA, and ET are not required.

• Proceedings of the Korean Society of Plant Pathology Conference
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• 1999.04a
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• pp.52-52
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• 1999

• Proceedings of the Korean Society of Plant Pathology Conference
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• 2003.10a
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• pp.68.1-68
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• 2003

When plants are infected by plant pathogens, typical disease symptom termed lesion, appears in compatible interaction. Whereas, in incompatible interactions, only small speck of lesions are visible on the leaf surfaces. Hypersensitive response (HR) of plant which is the result of infection by incompatible pathogens, is a well known defense response inducing rapid cell death resulting in complete resistance. However, some rice mutants show spontaneous disease symptoms during the growth stages without interaction with pathogens. We investigated the spontaneous cell death mutant called Blast Lesion Mimic(BLM) generated by EMS mutation, on the relationship with the hypersensitive response as well as resistant characteristics. Accumulation of phenolic compounds were detected around the lesions as lesions develop on leaf surface. Activation of PR gene was detected before the lesion appeared, and that result indicates the defense-related response are started earlier than lesion formation. The BLM mutant showed resistant response to inoculation of Magnaporthe grisea KJ201 with which the wild type Hwacheong is totally susceptible. Informations on the formation of spontaneous lesions and detail analysis of lesion mimic mutants and related genes are very limited to date. It is really important to understand the phenomenon of the defense-related lesion formation for developing resistant cultivar for rice blast pathogens

• Korean Journal of Agricultural Science
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• v.48 no.3
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• pp.643-654
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• 2021

Phytophthora capsici is one of the most destructive hemibiotrophic pathogens; it can cause blight in chili peppers, and secrete various effector proteins to infect the plants. These effectors contain an N-terminal conserved RXLR motif. Here, we generated full-length RXLR effector coding genes using primer pairs, and cloned them into the pGR106 vector for in planta expression. Two of these genes, PcREK6 and PcREK41 (P. capsici RXLR effector from the Korea isolate), were further characterized. PcREK6 and PcREK41 genes showed that they encode effector proteins with a general modular structure, including the N-terminal conserved RXLR-DEER motif and signal peptide sequences. PcREK6 and PcREK41 expressions were strongly induced when the chili pepper plants (Capsicum annuum) were challenged with P. capsici. These results provide molecular evidence to elucidate the virulence or avirulence factors in chili pepper. Our results also showed that two effectors induce hypersensitive response (HR) cell death when expressed in chili leaves. Cell death suppression assays in Nicotiana benthamiana revealed that most effectors could not suppress programmed cell death (PCD) triggered by Bcl-associated X (BAX) or Phytophthora infestans elicitin (INF1). However, PcREK6 fully suppressed PCD triggered by BAX, while PcREK41 partially suppressed PCD triggered by INF1 elicitin. These results suggest that PcREK effectors from P. capsici interact with putative resistance (R) proteins in planta, and different effectors may target different pathways in a plant cell to suppress pattern-triggered immunity (PTI) or effector-triggered immunity (ETI).

• Proceedings of the Korean Society of Plant Pathology Conference
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• 2003.10a
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• pp.72.1-72
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• 2003

Generally, plants defend themselves against pathogens by structural and biochemical reactions. Defense structures act as physical barriers and inhibit the pathogen from gaining entrance and spreading through the plant. Xanthomonas axonopodis pv glycines, the causal pathogen of bacterial pustule of soybean, causes hypersensitive response (HR). When pepper fruits were inoculated with X. axonopodis pv. glycines, in situ, time-series defense-related structural changes occurred in the inoculated sites. Early responses were programmed cell death (PCD), characterized by condensation and vacuolization of the cytoplasm, condensation of nuclear materials, and fragmentation of the nuclear DNA, which were observed by transmission electron microscopy. Nuclear fragmentation was proven by TUNEL method under confocal laser scanning microscopy and DNA laddering through eletrophoresis. At later stages, plant responses were cell elongation and cell division, forming a periderm-like boundary layer that demarcated healthy tissues from the inoculation sites. Using several stains such as toluidine blue, sudan IV, annexin V, and phloroglucinol-HCl, defense-related materials and structural changes were also examined.