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 Flagellin/TLR5 responses in epithelia reveal intertwined activation of inflammatory and apoptotic pathways

2006 ◽  
Vol 290 (1) ◽  
pp. G96-G108 ◽  
Author(s):  
Hui Zeng ◽  
Huixia Wu ◽  
Valerie Sloane ◽  
Rheinallt Jones ◽  
Yimin Yu ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Programmed Cell Death ◽  
Pathogenic Bacteria ◽  
Caspase Activation ◽  
Extrinsic Pathway ◽  
Tnf Α ◽  
Proinflammatory Responses ◽  
Apoptotic Pathways ◽  
Toll Like Receptor 5

Flagellin, the primary structural component of bacterial flagella, is recognized by Toll-like receptor 5 (TLR5) present on the basolateral surface of intestinal epithelial cells. Utilizing biochemical assays of proinflammatory signaling pathways and mRNA expression profiling, we found that purified flagellin could recapitulate the human epithelial cell proinflammatory responses activated by flagellated pathogenic bacteria. Flagellin-induced proinflammatory activation showed similar kinetics and gene specificity as that induced by the classical endogenous proinflammatory cytokine TNF-α, although both responses were more rapid than that elicited by viable flagellated bacteria. Flagellin, like TNF-α, activated a number of antiapoptotic mediators, and pretreatment of epithelial cells with this bacterial protein could protect cells from subsequent bacterially mediated apoptotic challenge. However, when NF-κB-mediated or phosphatidylinositol 3-kinase/Akt proinflammatory signaling was blocked, flagellin could induce programmed cell death. Consistently, we demonstrate that flagellin and viable flagellate Salmonella induces both the extrinsic and intrinsic caspase activation pathways, with the extrinsic pathway (caspase 8) activated by purified flagellin in a TLR5-dependant fashion. We conclude that interaction of flagellin with epithelial cells induces caspase activation in parallel with proinflammatory responses. Such intertwining of proinflammatory and apoptotic signaling mediated by bacterial products suggests roles for host programmed cell death in the pathogenesis of enteric infections.

scholarly journals XopQ induced stromule formation in Nicotiana benthamiana is causally linked to ETI signaling and depends on ADR1 and NRG1

2021 ◽  
Author(s):  
Jennifer Prautsch ◽  
Jessica L. Erickson ◽  
Sedef Özyürek ◽  
Rahel Gormannns ◽  
Lars Franke ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Nicotiana Benthamiana ◽  
Double Mutant ◽  
Plant Immunity ◽  
Signaling Cascade ◽  
Nuclear Dynamics ◽  
Hypersensitive Cell Death ◽  
Host Cell Death ◽  
Dependent Cell

In Nicotiana benthamiana, expression of the Xanthomonas effector XopQ triggers ROQ1-dependent ETI responses and in parallel accumulation of plastids around the nucleus and the formation of stromules. Both processes were proposed to contribute to ETI-related hypersensitive cell death and thereby to plant immunity. Whether these reactions are directly connected to ETI signaling events has not been tested. Here we utilized transient expression experiments to determine whether XopQ-mediated plastid reactions are a result of XopQ perception by ROQ1 or a consequence of XopQ virulence activity. We find that N. benthamiana mutants lacking ROQ1, both RNLs (NRG1 and ADR1) or EDS1, fail to elicit XopQ-dependent host cell death and stromule formation. Mutants lacking only NRG1 lost XopQ-dependent cell death but retained some stromule induction that was abolished in the RNL double mutant. This analysis aligns XopQ-induced stromules with the ETI signaling cascade but not to host programmed cell death. Furthermore, data reveal that XopQ-triggered plastid clustering is not strictly linked to stromule formation during ETI. Our data suggest that stromule formation, in contrast to chloroplast peri-nuclear dynamics, is an integral part of the N. benthamiana ETI response and that both RNL sub-types play a role in this ETI response.

Versinia pestis YopJ, YopT, and YopK coordinate programmed cell death and cytokine responses to promote pneumonic plague

2017 ◽  
Author(s):  
◽  
Rachel M. Olson
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Bacterial Growth ◽  
Cell Function ◽  
Immune Cell ◽  
Effector Proteins ◽  
University Of Missouri ◽  
Cellular Machinery ◽  
The University ◽  
Inflammatory Macrophages

[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] Yersinia pestis has been responsible for three major pandemics of plague, including the infamous Black Death that killed 250 million people in Europe. The disease progresses rapidly due to a combination of bacterial growth and host immunopathology. During infection, Y. pestis utilizes a type III secretion system (T3SS), which is essential for virulence, to inject effector proteins that disrupt immune cell function. The majority of the Yops are dedicated to the control of programmed cell death of immune cells, namely macrophages and neutrophils, and through this, it has been proposed that initially there is immune suppression followed by an acute inflammatory response that accelerates bacterial growth and disease. Recent work has focused on the inflammasome, cellular machinery that is activated upon insertion of the translocation pore that results in host cell lysis and the release of inflammatory cytokines. In this work, we defined a novel pathogenesis mechanism involving the activation of rapid lysis of inflammatory macrophages via necroptosis by injected bacterial effectors YopT and YopJ, each with cysteine protease activity. We show that YopT is a virulence factor for plague, while deletion of YopJ had no detectable impact on virulence. Further, we found that injection of catalytically inactive YopJ induces strong activation of the inflammasome and stimulates host defense against plague. YopK modulates the effects of YopT and YopJ. Overall, it appears that induction of necroptosis by YopT and YopJ subverts the activation of the inflammasome and contributes to pathogenesis of plague.

scholarly journals RIPK1-dependent apoptosis bypasses pathogen blockade of innate signaling to promote immune defense

2017 ◽  
Vol 214 (11) ◽  
pp. 3171-3182 ◽  
Author(s):  
Lance W. Peterson ◽  
Naomi H. Philip ◽  
Alexandra DeLaney ◽  
Meghan A. Wynosky-Dolfi ◽  
Kendra Asklof ◽  
...  
Keyword(s):  
Cell Death ◽  
Kinase Activity ◽  
Cytokine Production ◽  
Mapk Signaling ◽  
Immune Defense ◽  
Effector Proteins ◽  
Host Cells ◽  
Effector Triggered Immunity ◽  
Induced Apoptosis

Many pathogens deliver virulence factors or effectors into host cells in order to evade host defenses and establish infection. Although such effector proteins disrupt critical cellular signaling pathways, they also trigger specific antipathogen responses, a process termed “effector-triggered immunity.” The Gram-negative bacterial pathogen Yersinia inactivates critical proteins of the NF-κB and MAPK signaling cascade, thereby blocking inflammatory cytokine production but also inducing apoptosis. Yersinia-induced apoptosis requires the kinase activity of receptor-interacting protein kinase 1 (RIPK1), a key regulator of cell death, NF-κB, and MAPK signaling. Through the targeted disruption of RIPK1 kinase activity, which selectively disrupts RIPK1-dependent cell death, we now reveal that Yersinia-induced apoptosis is critical for host survival, containment of bacteria in granulomas, and control of bacterial burdens in vivo. We demonstrate that this apoptotic response provides a cell-extrinsic signal that promotes optimal innate immune cytokine production and antibacterial defense, demonstrating a novel role for RIPK1 kinase–induced apoptosis in mediating effector-triggered immunity to circumvent pathogen inhibition of immune signaling.

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 Phytophthora sojae TatD Nuclease Positively Regulates Sporulation and Negatively Regulates Pathogenesis

2014 ◽  
Vol 27 (10) ◽  
pp. 1070-1080 ◽  
Author(s):  
Linlin Chen ◽  
Danyu Shen ◽  
Nannan Sun ◽  
Jing Xu ◽  
Wen Wang ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Functional Analysis ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Dna Degradation ◽  
Phytophthora Sojae ◽  
Zoospore Production ◽  
Basic Biology ◽  
Eukaryotic Microbes

During pathogenic interactions, both the host and pathogen are exposed to conditions that induce programmed cell death (PCD). Certain aspects of PCD have been recently examined in eukaryotic microbes but not in oomycetes. Here, we identified conserved TatD proteins in Phytophthora sojae; the proteins are key components of DNA degradation in apoptosis. We selected PsTatD4 for further investigation because the enzyme is unique to the oomycete branch of the phylogenetic tree. The purified protein exhibited DNase activity in vitro. Its expression was upregulated in sporangia and later infective stages but downregulated in cysts and during early infection. Functional analysis revealed that the gene was required for sporulation and zoospore production, and the expression levels were associated with the numbers of hydrogen-peroxide-induced terminal dUTP nick end-labeling-positive cells. Furthermore, overexpression of PsTatD4 gene reduced the virulence in a susceptible soybean cultivar. Together, these data suggest that apoptosis may play different roles in the early and late infective stages of P. sojae, and that PsTatD4 is a key regulator of infection. The association of PsTatD4 and apoptosis will lay a foundation to understanding the basic biology of apoptosis and its roles in P. sojae disease cycle.

scholarly journals The type III effector HopF2Pto targets Arabidopsis RIN4 protein to promote Pseudomonas syringae virulence

2010 ◽  
Vol 107 (5) ◽  
pp. 2349-2354 ◽  
Author(s):  
Mike Wilton ◽  
Rajagopal Subramaniam ◽  
James Elmore ◽  
Corinna Felsensteiner ◽  
Gitta Coaker ◽  
...  
Keyword(s):  
Pseudomonas Syringae ◽  
Plant Immunity ◽  
Effector Proteins ◽  
Type Iii ◽  
Pathogen Effector ◽  
Effector Triggered Immunity ◽  
Type Iii Secretion Effector ◽  
Virulence Target

Plant immunity can be induced by two major classes of pathogen-associated molecules. Pathogen- or microbe-associated molecular patterns (PAMPs or MAMPs) are conserved molecular components of microbes that serve as “non-self” features to induce PAMP-triggered immunity (PTI). Pathogen effector proteins used to promote virulence can also be recognized as “non-self” features or induce a “modified-self” state that can induce effector-triggered immunity (ETI). The Arabidopsis protein RIN4 plays an important role in both branches of plant immunity. Three unrelated type III secretion effector (TTSE) proteins from the phytopathogen Pseudomonas syringae, AvrRpm1, AvrRpt2, and AvrB, target RIN4, resulting in ETI that effectively restricts pathogen growth. However, no pathogenic advantage has been demonstrated for RIN4 manipulation by these TTSEs. Here, we show that the TTSE HopF2Pto also targets Arabidopsis RIN4. Transgenic plants conditionally expressing HopF2Pto were compromised for AvrRpt2-induced RIN4 modification and associated ETI. HopF2Pto interfered with AvrRpt2-induced RIN4 modification in vitro but not with AvrRpt2 activation, suggestive of RIN4 targeting by HopF2Pto. In support of this hypothesis, HopF2Pto interacted with RIN4 in vitro and in vivo. Unlike AvrRpm1, AvrRpt2, and AvrB, HopF2Pto did not induce ETI and instead promoted P. syringae growth in Arabidopsis. This virulence activity was not observed in plants genetically lacking RIN4. These data provide evidence that RIN4 is a major virulence target of HopF2Pto and that a pathogenic advantage can be conveyed by TTSEs that target RIN4.

scholarly journals Genome-wide analysis uncovers tomato leaf lncRNAs transcriptionally active upon Pseudomonas syringae pv. tomato challenge

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hernan G. Rosli ◽  
Emilia Sirvent ◽  
Florencia N. Bekier ◽  
Romina N. Ramos ◽  
Marina A. Pombo
Keyword(s):  
Pseudomonas Syringae ◽  
Pathogenic Bacteria ◽  
Direct Detection ◽  
Effector Proteins ◽  
Surface Pattern ◽  
Large Set ◽  
Protein Coding ◽  
Genome Wide ◽  
Effector Triggered Immunity ◽  
Molecular Patterns

AbstractPlants rely on (in)direct detection of bacterial pathogens through plasma membrane-localized and intracellular receptor proteins. Surface pattern-recognition receptors (PRRs) participate in the detection of microbe-associated molecular patterns (MAMPs) and are required for the activation of pattern-triggered immunity (PTI). Pathogenic bacteria, such as Pseudomonas syringae pv. tomato (Pst) deploys ~ 30 effector proteins into the plant cell that contribute to pathogenicity. Resistant plants are capable of detecting the presence or activity of effectors and mount another response termed effector-triggered immunity (ETI). In order to investigate the involvement of tomato’s long non-coding RNAs (lncRNAs) in the immune response against Pst, we used RNA-seq data to predict and characterize those that are transcriptionally active in leaves challenged with a large set of treatments. Our prediction strategy was validated by sequence comparison with tomato lncRNAs described in previous works and by an alternative approach (RT-qPCR). Early PTI (30 min), late PTI (6 h) and ETI (6 h) differentially expressed (DE) lncRNAs were identified and used to perform a co-expression analysis including neighboring (± 100 kb) DE protein-coding genes. Some of the described networks could represent key regulatory mechanisms of photosynthesis, PRR abundance at the cell surface and mitigation of oxidative stress, associated to tomato-Pst pathosystem.

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