• Molecules and Cells
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• v.42 no.7
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• pp.503-511
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• 2019

As sessile organisms, plants have developed sophisticated system to defend themselves against microbial attack. Since plants do not have specialized immune cells, all plant cells appear to have the innate ability to recognize pathogens and turn on an appropriate defense response. The plant innate immune system has two major branches: PAMPs (pathogen associated molecular patterns)-triggered immunity (PTI) and effector-triggered immunity (ETI). The ability to discriminate between self and non-self is a fundamental feature of living organisms, and it is a prerequisite for the activation of plant defenses specific to microbial infection. Arabidopsis cells express receptors that detect extracellular molecules or structures of the microbes, which are called collectively PAMPs and activate PTI. However, nucleotidebinding site leucine-rich repeats (NB-LRR) proteins mediated ETI is induced by direct or indirect recognition of effector molecules encoded by avr genes. In Arabidopsis, plasmamembrane localized multifunctional protein RIN4 (RPM1-interacting protein 4) plays important role in both PTI and ETI. Previous studies have suggested that RIN4 functions as a negative regulator of PTI. In addition, many different bacterial effector proteins modify RIN4 to destabilize plant immunity and several NB-LRR proteins, including RPM1 (resistance to Pseudomonas syringae pv. maculicola 1), RPS2 (resistance to P. syringae 2) guard RIN4. This review summarizes the current studies that have described signaling mechanism of RIN4 function, modification of RIN4 by bacterial effectors and different interacting partner of RIN4 in defense related pathway. In addition, the emerging role of the RIN4 in plant physiology and intercellular signaling as it presents in exosomes will be discussed.

• 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).

• The Plant Pathology Journal
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• v.26 no.3
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• pp.209-215
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• 2010

Plant pathogenic oomycetes, such as Phytophthora spp., are the causal agent of the most devastating plant diseases. During infection, these pathogens accomplish parasitic colonization of plants by modulating host defenses through an array of disease effector proteins. These effectors are classified in two classes based on their target sites in the host plant. Apoplastic effectors are secreted into the plant extracellular space, and cytoplasmic effectors are translocated inside the plant cell, through the haustoria that enter inside living host cell. Recent characterization of some oomycete Avr genes showed that they encode effector protein with general modular structure including N-terminal conserved RXLR-DEER motif. More detailed evidences suggest that these AVR effectors are secreted by the pathogenic oomycetes and then translocated into the host plant cell during infection. Recent findings indicated that one of the P. infestans effector, Avrblb2, specifically induces hypersensitive response (HR) in the presence of Solanum bulbocastanum late blight resistance genes Rpi-blb2. On the other hand, another secreted RXLR protein PexRD8 originated from P. infestans suppressed the HCD triggered by the elicitin INF1. In this review, we described recent progress in characterized RXLR effectors in Phytophthora spp. and their dual functions as modulators of host plant immunity.

• Molecules and Cells
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• v.39 no.5
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• pp.426-438
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• 2016

Plant disease resistance occurs as a hypersensitive response (HR) at the site of attempted pathogen invasion. This specific event is initiated in response to recognition of pathogen-associated molecular pattern (PAMP) and subsequent PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI). Both PTI and ETI mechanisms are tightly connected with reactive oxygen species (ROS) production and disease resistance that involves distinct biphasic ROS production as one of its pivotal plant immune responses. This unique oxidative burst is strongly dependent on the resistant cultivars because a monophasic ROS burst is a hallmark of the susceptible cultivars. However, the cause of the differential ROS burst remains unknown. In the study here, we revealed the plausible underlying mechanism of the differential ROS burst through functional understanding of the Magnaporthe oryzae (M. oryzae) AVR effector, AVR-Pii. We performed yeast two-hybrid (Y2H) screening using AVR-Pii as bait and isolated rice NADP-malic enzyme2 (Os-NADP-ME2) as the rice target protein. To our surprise, deletion of the rice Os-NADP-ME2 gene in a resistant rice cultivar disrupted innate immunity against the rice blast fungus. Malic enzyme activity and inhibition studies demonstrated that AVR-Pii proteins specifically inhibit in vitro NADP-ME activity. Overall, we demonstrate that rice blast fungus, M. oryzae attenuates the host ROS burst via AVR-Pii-mediated inhibition of Os-NADP-ME2, which is indispensable in ROS metabolism for the innate immunity of rice. This characterization of the regulation of the host oxidative burst will help to elucidate how the products of AVR genes function associated with virulence of the pathogen.

• ALGAE
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• v.38 no.4
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• pp.203-215
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• 2023

Oomycete pathogens are one of the most serious threats to the rapidly growing global algae aquaculture industry but research into how they spread and how algae respond to infection is unresolved, let alone a proper classification of the pathogens. Even the taxonomy of the genera Pythium and Olpidiopsis, which contain the most economically damaging pathogens in red algal aquaculture, and are among the best studied, needs urgent clarification, as existing morphological classifications and molecular evidence are often inconsistent. Recent studies have reported a number of genes involved in defense responses against oomycete pathogens in red algae, including pattern-triggered immunity and effector-triggered immunity. Accumulating evidence also suggests that calcium-mediated reactive oxygen species signaling plays an important role in the response of red algae to oomycete pathogens. Current management strategies to control oomycete pathogens in aquaculture are based on the high resistance of red algae to abiotic stress, these have environmental consequences and are not fully effective. Here, we compile a revised list of oomycete pathogens known to infect marine red algae and outline the current taxonomic situation. We also review recent research on the molecular and cellular responses of red algae to oomycete infection that has only recently begun, and outline the methods currently used to control disease in the field.

• Korean Journal of Agricultural Science
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• v.45 no.4
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• pp.561-573
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• 2018

Oomycetes are known to secrete a vast arsenal of effectors that modulate the host defense system as well as facilitate establishing a parasitic infection in plants. In recent years, tremendous progress has been made in the field of effectromics based on studies of oomycetes, especially the cytoplasmic family of RXLR effectors. Yet, the biology of the RXLR effector family is still poorly understood. There has been a consensus regarding the structure of the RXLR motif in the mycologist community. However, the function of the RXLR motif is still unclear. First, different models have suggested that the role of the RXLR motif is either in translocation to a target destination inside a host cell or in the cleavage of itself followed by secretion. Second, recent studies have suggested different functional models for the RXLR motif. According to a widely accepted model, the RXLR motif is directly involved in the translocation of effectors to target sites. In contrast, a new study has proposed that the RXLR motif is involved in secretion rather than translocation. Thus, this review is an attempt to summarize the recent advances made in the functional analysis of the N-terminal domain of RXLR effectors.

• 한국균학회소식:학술대회논문집
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• 2015.11a
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• pp.26-26
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• 2015

Phytophthora infestans is the causal agent of potato and tomato late blight, one of the most devastating plant diseases. P. infestans secretes effector proteins that are both modulators and targets of host plant immunity. Among these are the so-called RXLR effectors that function inside plant cells and are characterized by a conserved motif following the N-terminal signal peptide. In contrast, the effector activity is encoded by the C terminal region that follows the RXLR domain. Recently, I performed in planta functional profiling of different RXLR effector alleles. These genes were amplified from a variety of P. infestans isolates and cloned into a Potato virus X (PVX) vector for transient in planta expression. I assayed for R-gene specific induction of hypersensitive cell death. The findings included the discovery of new effector with avirulence activity towards the Solanum bulbocastanum Rpi-blb2 resistance gene. The Rpi-blb2 encodes a protein with a putative CC-NBS-LRR (a coiled-coil-nucleotide binding site and leucine-rich repeat) motif that confers Phytophthora late blight disease resistance. We examined the components required for Rpi-blb2-mediated resistance to P. infestans in Nicotiana benthamiana. Virus-induced gene silencing was used to repress candidate genes in N. benthamiana and to assay against P. infestans infections. NbSGT1 was required for disease resistance to P. infestans and hypersensitive responses (HRs) triggered by co-expression of AVRblb2 and Rpi-blb2 in N. benthamiana. RAR1 and HSP90 did not affect disease resistance or HRs in Rpi-blb2-transgenic plants. To elucidate the role of salicylic acid (SA) in Rpi-blb2-mediated resistance, we analyzed the response of NahG-transgenic plants following P. infestans infection. The increased susceptibility of Rpi-blb2-transgenic plants in the NahG background correlated with reduced SA and SA glucoside levels. Furthermore, Rpi-blb2-mediated HR cell death was associated with $H_2O_2$, but not SA, accumulation. SA affects basal defense and Rpi-blb2-mediated resistance against P. infestans. These findings provide evidence about the roles of SGT1 and SA signaling in Rpi-blb2-mediated resistance against P. infestans.

• Journal of Microbiology and Biotechnology
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• v.29 no.12
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• pp.1975-1981
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• 2019

Recently, outbreaks of food-borne diseases linked to fresh produce have been an emerging public health concern worldwide. Previous research has shown that when human pathogens co-exist with plant pathogens, they have improved growth and survival rates. In this study, we have assessed whether Escherichia coli O157:H7 benefits from the existence of a phytopathogenic bacterium and the underlying mechanisms were further investigated. When Pseudomonas syringae pv. tomato DC3000 (Pst DC3000) and E. coli O157:H7 were co-inoculated by either dipping or infiltration methods, the populations of E. coli O157:H7 increased; however, no effect was observed when type three secretion system (T3SS) mutants were used instead, suggesting that E. coli O157:H7 benefits from the presence of Pst DC3000. In addition, this study confirmed that the E. coli O157:H7 populations increased when they occupied the tomato leaf intercellular space; this colonization of the interior of the leaves was possible due to the suppression of the PAMP-triggered immunity (PTI) by Pst DC3000, in particular with the AvrPto effector. In conclusion, our data support a plausible model that E. coli O157:H7 benefits from the presence of Pst DC3000 via AvrPto suppression of the PTI resistance.

• The Plant Pathology Journal
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• v.33 no.2
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• pp.163-169
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• 2017

$SIMAPKKK{\alpha}$, a tomato (Solanum lycopersicum) mitogen-activated protein kinase kinase kinase, is a positive regulator of Pto-mediated effector-triggered immunity, which elicits programmed cell death (PCD) in plants. In this study, we examined whether putative phosphorylation sites in the conserved activation segment of the $SIMAPKKK{\alpha}$ kinase domain are critical for eliciting PCD. Three amino acids, $threonine^{353}$, $serine^{360}$ ($Ser^{360}$), or $serine^{364}$ ($Ser^{364}$), in the conserved activation segment of $SIMAPKKK{\alpha}$ kinase domain were substituted to alanine (T353A, S360A, or S364A), and these variants were transiently expressed in tomato and Nicotiana benthamiana plants. Two alanine substitutions, S360A and S364A, completely abolished $SIMAPKKK{\alpha}$ PCD-eliciting activity in both plants, while T353A substitution did not affect its PCD-eliciting activity. $SIMAPKKK{\alpha}$ wild type and variant proteins accumulated to similar levels in plant leaves. However, $SIMAPKKK{\alpha}$ protein with the largest size was missed when either S360A or S364A substitutions were expressed, whereas proteins with the smaller masses were more accumulated than those of full-length of $SIMAPKKK{\alpha}$ and T353A. These results suggest that phosphorylation of $SIMAPKKK{\alpha}$ at $Ser^{360}$ and $Ser^{364}$ is critical for PCD elicitation in plants.

• Molecules and Cells
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• v.42 no.9
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• pp.637-645
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• 2019

Effector-triggered immunity (ETI) is an effective layer of plant defense initiated upon recognition of avirulence (Avr) effectors from pathogens by cognate plant disease resistance (R) proteins. In rice, a large number of R genes have been characterized from various cultivars and have greatly contributed to breeding programs to improve resistance against the rice blast pathogen Magnaporthe oryzae. The extreme diversity of R gene repertoires is thought to be a result of co-evolutionary history between rice and its pathogens including M. oryzae. Here we show that Pii is an allele of Pi5 by DNA sequence characterization and complementation analysis. Pii-1 and Pii-2 cDNAs were cloned by reverse transcription polymerase chain reaction from the Pii-carrying cultivar Fujisaka5. The complementation test in susceptible rice cultivar Dongjin demonstrated that the rice blast resistance mediated by Pii, similar to Pi5, requires the presence of two nucleotide-binding leucine-rich repeat genes, Pii-1 and Pii-2. Consistent with our hypothesis that Pi5 and Pii are functionally indistinguishable, the replacement of Pii-1 by Pi5-1 and Pii-2 by Pi5-2, respectively, does not change the level of disease resistance to M. oryzae carrying AVR-Pii. Surprisingly, Exo70F3, required for Pii-mediated resistance, is dispensable for Pi5-mediated resistance. Based on our results, despite similarities observed between Pi5 and Pii, we hypothesize that Pi5 and Pii pairs require partially distinct mechanisms to function.