scholarly journals sORF-encoded polypeptide SEP1 is a novel virulence factor of Phytophthora pathogens

2020 ◽  
Author(s):  
Nan Wang ◽  
Zhiyuan Yin ◽  
Weiwei Duan ◽  
Xiong Zhang ◽  
Lei Pi ◽  
...  
Keyword(s):  
Cell Death ◽  
Virulence Factor ◽  
Nicotiana Benthamiana ◽  
Phytophthora Species ◽  
Effector Proteins ◽  
Economic Losses ◽  
Reading Frame ◽  
C Terminus ◽  
Environmental Responses ◽  
Small Open Reading Frame

Diseases caused by the notorious Phytophthora species result in enormous economic losses to crops and forests. Increasing evidence suggests that small open reading frame-encoded polypeptides (SEPs) participate in environmental responses of animals, plants, and fungi. However, it remains largely unknown whether Phytophthora pathogens produce SEPs. Here, we systematically predicted and identified 96 SEP candidates in P. capsici. Among them, three may induce stable cell death in Nicotiana benthamiana. Phytophthora-specific and conserved SEP1 facilitated P. capsici infection. PcSEP1-induced cell death is BAK1- and SOBIR1-independent and is correlated to its virulence function. Finally, PcSEP1 may be targeted to the apoplast for carrying out its functions, for which the C-terminus is indispensable. Together, our results demonstrated that SEP1 is a new virulence factor, and previously unknown SEPs may act as effector proteins in Phytophthora pathogens.

scholarly journals WtsE, an AvrE-Family Effector Protein from Pantoea stewartii subsp. stewartii, Causes Disease-Associated Cell Death in Corn and Requires a Chaperone Protein for Stability

2006 ◽  
Vol 19 (10) ◽  
pp. 1092-1102 ◽  
Author(s):  
Jong Hyun Ham ◽  
Doris R. Majerczak ◽  
Angel S. Arroyo-Rodriguez ◽  
David M. Mackey ◽  
David L. Coplin
Keyword(s):  
Cell Death ◽  
Sweet Corn ◽  
Coli Strain ◽  
Effector Proteins ◽  
Erwinia Chrysanthemi ◽  
Endoplasmic Reticulum Membrane ◽  
E Coli ◽  
Pantoea Stewartii ◽  
C Terminus ◽  
Efficient Delivery

The pathogenicity of Pantoea stewartii subsp. stewartii to sweet corn and maize requires a Hrp type III secretion system. In this study, we genetically and functionally characterized a disease-specific (Dsp) effector locus, composed of wtsE and wtsF, that is adjacent to the hrp gene cluster. WtsE, a member of the AvrE family of effector proteins, was essential for pathogenesis on corn and was complemented by DspA/E from Erwinia amylovora. An intact C-terminus of WtsE, which contained a putative endoplasmic reticulum membrane retention signal, was important for function of WtsE. Delivery of WtsE into sweet corn leaves by an Escherichia coli strain carrying the hrp cluster of Erwinia chrysanthemi caused water-soaking and necrosis. WtsE-induced cell death was not inhibited by cycloheximide treatment, unlike the hypersensitive response caused by a known Avr protein, AvrRxo1. WtsF, the putative chaperone of WtsE, was not required for secretion of WtsE from P. stewartii, and the virulence of wtsF mutants was reduced only at low inoculum concentrations. However, WtsF was required for full accumulation of WtsE within the bacteria at low temperatures. In contrast, WtsF was needed for efficient delivery of WtsE from E. coli via the Erwinia chrysanthemi Hrp system.

scholarly journals Pseudomonas Type III Effector AvrPto Suppresses the Programmed Cell Death Induced by Two Nonhost Pathogens in Nicotiana benthamiana and Tomato

2004 ◽  
Vol 17 (12) ◽  
pp. 1328-1336 ◽  
Author(s):  
Li Kang ◽  
Xiaoyan Tang ◽  
Kirankumar S. Mysore
Keyword(s):  
Cell Death ◽  
Disease Resistance ◽  
Programmed Cell Death ◽  
Pseudomonas Syringae ◽  
Type Iii Secretion ◽  
Nicotiana Benthamiana ◽  
Effector Proteins ◽  
Type Iii ◽  
Bacterial Pathogenicity ◽  
Suppression Effects

Many gram-negative bacterial pathogens rely on a type III secretion system to deliver a number of effector proteins into the host cell. Though a number of these effectors have been shown to contribute to bacterial pathogenicity, their functions remain elusive. Here we report that AvrPto, an effector known for its ability to interact with Pto and induce Pto-mediated disease resistance, inhibited the hypersensitive response (HR) induced by nonhost pathogen interactions. Pseudomonas syringae pv. tomato T1 causes an HR-like cell death on Nicotiana benthamiana. This rapid cell death was delayed significantly in plants inoculated with P. syringae pv. tomato expressing avrPto. In addition, P. syringae pv. tabaci expressing avrPto suppressed nonhost HR on tomato prf3 and ptoS lines. Transient expression of avrPto in both N. benthamiana and tomato prf3 plants also was able to suppress nonhost HR. Interestingly, AvrPto failed to suppress cell death caused by other elicitors and nonhost pathogens. AvrPto also failed to suppress cell death caused by certain gene-for-gene disease resistance interactions. Experiments with avrPto mutants revealed several residues important for the suppression effects. AvrPto mutants G2A, G99V, P146L, and a 12-amino-acid C-terminal deletion mutant partially lost the suppression ability, whereas S94P and I96T enhanced suppression of cell death in N. benthamiana. These results, together with other discoveries, demonstrated that suppression of host-programmed cell death may serve as one of the strategies bacterial pathoens use for successful invasion.

scholarly journals Identification and Functional Analysis of AopN, an Acidovorax Citrulli Effector that Induces Programmed Cell Death in Plants

2020 ◽  
Vol 21 (17) ◽  
pp. 6050 ◽  
Author(s):  
Xiaoxiao Zhang ◽  
Mei Zhao ◽  
Jie Jiang ◽  
Linlin Yang ◽  
Yuwen Yang ◽  
...  
Keyword(s):  
Functional Analysis ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Pathogenic Bacteria ◽  
Plant Immunity ◽  
Effector Proteins ◽  
Economic Losses ◽  
Homologous Protein ◽  
Acidovorax Citrulli ◽  
Effector Triggered Immunity

Bacterial fruit blotch (BFB), caused by Acidovorax citrulli, seriously affects watermelon and other cucurbit crops, resulting in significant economic losses. However, the pathogenicity mechanism of A. citrulli is not well understood. Plant pathogenic bacteria often suppress the plant immune response by secreting effector proteins. Thus, identifying A. citrulli effector proteins and determining their functions may improve our understanding of the underlying pathogenetic mechanisms. In this study, a novel effector, AopN, which is localized on the cell membrane of Nicotiana benthamiana, was identified. The functional analysis revealed that AopN significantly inhibited the flg22-induced reactive oxygen species burst. AopN induced a programmed cell death (PCD) response. Unlike its homologous protein, the ability of AopN to induce PCD was dependent on two motifs of unknown functions (including DUP4129 and Cpta_toxin), but was not dependent on LXXLL domain. More importantly, the virulence of the aopN mutant of A. citrulli in N. benthamiana significantly decreased, indicating that it was a core effector. Further analysis revealed that AopN interacted with watermelon ClHIPP and ClLTP, which responds to A. citrulli strain Aac5 infection at the transcription level. Collectively, these findings indicate that AopN suppresses plant immunity and activates the effector-triggered immunity pathway.

scholarly journals Phytophthora parasitica Effector PpRxLR2 Suppresses Nicotiana benthamiana Immunity

2018 ◽  
Vol 31 (4) ◽  
pp. 481-493 ◽  
Author(s):  
R. J. D. Dalio ◽  
H. J. Maximo ◽  
T. S. Oliveira ◽  
R. O. Dias ◽  
M. C. Breton ◽  
...  
Keyword(s):  
Nicotiana Benthamiana ◽  
Control Strategies ◽  
Functional Characterization ◽  
Phytophthora Species ◽  
Effector Proteins ◽  
Phytophthora Parasitica ◽  
In Planta ◽  
Bioinformatics Pipeline ◽  
Rxlr Effectors

Phytophthora species secrete several classes of effector proteins during interaction with their hosts. These proteins can have multiple functions including modulation of host physiology and immunity. The RxLR effectors have the ability to enter plant cells using the plant machinery. Some of these effectors have been characterized as immunity suppressors; however, very little is known about their functions in the interaction between Phytophthora parasitica and its hosts. Using a bioinformatics pipeline, we have identified 172 candidate RxLR effectors (CREs) in the isolate IAC 01_95 of P. parasitica. Of these 172 CREs, 93 were found to be also present in eight other genomes of P. parasitica, isolated from different hosts and continents. After transcriptomics and gene expression analysis, we have found five CREs to be up-regulated in in-vitro and in-planta samples. Subsequently, we selected three CREs for functional characterization in the model plant Nicotiana benthamiana. We show that PpRxLR2 is able to completely suppress INF-1-induced cell death, whereas PpRxLR3 and PpRxLR5 moderately suppressed N. benthamiana immunity in a less-extensive manner. Moreover, we confirmed the effector-triggered susceptibility activity of these proteins after transient transformation and infection of N. benthamiana plants. All three CREs enhanced virulence of P. parasitica during the interaction with N. benthamiana. These effectors, in particular PpRxLR2, can be targeted for the development of biotechnology-based control strategies of P. parasitica diseases.

scholarly journals Predication of the Effector Proteins Secreted by Fusarium sacchari Using Genomic Analysis and Heterogenous Expression

2022 ◽  
Vol 8 (1) ◽  
pp. 59
Author(s):  
Zhen Huang ◽  
Huixue Li ◽  
Yuming Zhou ◽  
Yixue Bao ◽  
Zhenzhen Duan ◽  
...  
Keyword(s):  
Cell Death ◽  
Fungal Infections ◽  
Expression Profiles ◽  
Expression System ◽  
Pathogenic Fungi ◽  
Effector Proteins ◽  
Economic Losses ◽  
Effector Molecules ◽  
Pathogen Effector ◽  
Fusarium Sacchari

One of the causative agents of pokkah boeng disease (PBD), which affects sugarcane crops globally, is the fungus Fusarium sacchari. These fungal infections reduce sugar quality and yield, resulting in severe economic losses. Effector proteins play important roles in the interactions between pathogenic fungi and plants. Here, we used bioinformatic prediction approaches to identify 316 candidate secreted effector proteins (CSEPs) in the complete genome of F. sacchari. In total, 95 CSEPs contained known conserved structures, representing 40 superfamilies and 18 domains, while an additional 91 CSEPs contained seven known motifs. Of the 130 CSEPs containing no known domains or motifs, 14 contained one of four novel motifs. A heterogeneous expression system in Nicotiana benthamiana was used to investigate the functions of 163 CSEPs. Seven CSEPs suppressed BAX-triggered programmed cell death in N. benthamiana, while four caused cell death in N. benthamiana. The expression profiles of these eleven CSEPs during F. sacchari infection suggested that they may be involved in sugarcane-F. sacchari interaction. Our results establish a basis for further studies of the role of effector molecules in pathogen–sugarcane interactions, and provide a framework for future predictions of pathogen effector molecules.

scholarly journals Interaction of Phytophthora sojae Effector Avr1b With E3 Ubiquitin Ligase GmPUB1 Is Required for Recognition by Soybeans Carrying Phytophthora Resistance Rps1-b and Rps1-k Genes

2021 ◽  
Vol 12 ◽  
Author(s):  
Shan Li ◽  
Regina Hanlon ◽  
Hua Wise ◽  
Narinder Pal ◽  
Hargeet Brar ◽  
...  
Keyword(s):  
Cell Death ◽  
Phytophthora Sojae ◽  
Effector Proteins ◽  
Host Cells ◽  
Bimolecular Fluorescence Complementation ◽  
Yeast Two Hybrid ◽  
Synonymous Mutations ◽  
Rxlr Effectors ◽  
C Terminus ◽  
Two Hybrid

Phytophthora sojae is an oomycete that causes stem and root rot disease in soybean. P. sojae delivers many RxLR effector proteins, including Avr1b, into host cells to promote infection. We show here that Avr1b interacts with the soybean U-box protein, GmPUB1-1, in yeast two-hybrid, pull down, and bimolecular fluorescence complementation (BIFC) assays. GmPUB1-1, and a homeologous copy GmPUB1-2, are induced by infection and encode 403 amino acid proteins with U-Box domains at their N-termini. Non-synonymous mutations in the Avr1b C-terminus that abolish suppression of cell death also abolished the interaction of Avr1b with GmPUB1-1, while deletion of the GmPUB1-1 C-terminus, but not the U box, abolished the interaction. BIFC experiments suggested that the GmPUB1-1-Avr1b complex is targeted to the nucleus. In vitro ubiquitination assays demonstrated that GmPUB1-1 possesses E3 ligase activity. Silencing of the GmPUB1 genes in soybean cotyledons resulted in loss of recognition of Avr1b by gene products encoded by Rps1-b and Rps1-k. The recognition of Avr1k (which did not interact with GmPUB1-1) by Rps1-k plants was not, however, affected following GmPUB1-1 silencing. Furthermore, over-expression of GmPUB1-1 in particle bombardment experiments triggered cell death suggesting that GmPUB1 may be a positive regulator of effector-triggered immunity. In a yeast two-hybrid system, GmPUB1-1 also interacted with a number of other RxLR effectors including Avr1d, while Avr1b and Avr1d interacted with a number of other infection-induced GmPUB proteins, suggesting that the pathogen uses a multiplex of interactions of RxLR effectors with GmPUB proteins to modulate host immunity.

scholarly journals Chinese Giant Salamander (Andrias davidianus) Iridovirus Infection Leads to Apoptotic Cell Death through Mitochondrial Damage, Caspases Activation, and Expression of Apoptotic-Related Genes

2019 ◽  
Vol 20 (24) ◽  
pp. 6149 ◽  
Author(s):  
Yiqun Li ◽  
Nan Jiang ◽  
Yuding Fan ◽  
Yong Zhou ◽  
Wenzhi Liu ◽  
...  
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Mitochondrial Damage ◽  
Apoptotic Cell Death ◽  
Economic Losses ◽  
P53 Expression ◽  
Andrias Davidianus ◽  
Chinese Giant Salamander ◽  
Infected Cells ◽  
Apoptotic Genes

Chinese giant salamander iridovirus (GSIV) is the causative pathogen of Chinese giant salamander (Andrias davidianus) iridovirosis, leading to severe infectious disease and huge economic losses. However, the infection mechanism by GSIV is far from clear. In this study, a Chinese giant salamander muscle (GSM) cell line is used to investigate the mechanism of cell death during GSIV infection. Microscopy observation and DNA ladder analysis revealed that DNA fragmentation happens during GSIV infection. Flow cytometry analysis showed that apoptotic cells in GSIV-infected cells were significantly higher than that in control cells. Caspase 8, 9, and 3 were activated in GSIV-infected cells compared with the uninfected cells. Consistently, mitochondria membrane potential (MMP) was significantly reduced, and cytochrome c was released into cytosol during GSIV infection. p53 expression increased at an early stage of GSIV infection and then slightly decreased late in infection. Furthermore, mRNA expression levels of pro-apoptotic genes participating in the extrinsic and intrinsic pathway were significantly up-regulated during GSIV infection, while those of anti-apoptotic genes were restrained in early infection and then rose in late infection. These results collectively indicate that GSIV induces GSM apoptotic cell death involving mitochondrial damage, caspases activation, p53 expression, and pro-apoptotic molecules up-regulation.

scholarly journals Detection of Rhodococcus fascians, the Causative Agent of Lily Fasciation in South Korea

Pathogens ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 241
Author(s):  
Joon Moh Park ◽  
Jachoon Koo ◽  
Se Won Kang ◽  
Sung Hee Jo ◽  
Jeong Mee Park
Keyword(s):  
Phylogenetic Analysis ◽  
South Korea ◽  
Nicotiana Benthamiana ◽  
Economic Value ◽  
Virulence Gene ◽  
Economic Losses ◽  
Herbaceous Perennials ◽  
Rhodococcus Fascians ◽  
Different Strains

Rhodococcus fascians is an important pathogen that infects various herbaceous perennials and reduces their economic value. In this study, we examined R. fascians isolates carrying a virulence gene from symptomatic lily plants grown in South Korea. Phylogenetic analysis using the nucleotide sequences of 16S rRNA, vicA, and fasD led to the classification of the isolates into four different strains of R. fascians. Inoculation of Nicotiana benthamiana with these isolates slowed root growth and resulted in symptoms of leafy gall. These findings elucidate the diversification of domestic pathogenic R. fascians and may lead to an accurate causal diagnosis to help reduce economic losses in the bulb market.

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