scholarly journals Effector-Triggered and Pathogen-Associated Molecular Pattern–Triggered Immunity Differentially Contribute to Basal Resistance to Pseudomonas syringae

2010 ◽  
Vol 23 (7) ◽  
pp. 940-948 ◽  
Author(s):  
Jie Zhang ◽  
Haibin Lu ◽  
Xinyan Li ◽  
Yan Li ◽  
Haitao Cui ◽  
...  
Keyword(s):  
Pseudomonas Syringae ◽  
Type Iii Secretion ◽  
Nonhost Resistance ◽  
Basal Resistance ◽  
Resistance Proteins ◽  
Pathogen Effectors ◽  
Molecular Pattern ◽  
Effector Triggered Immunity ◽  
Pathogen Associated Molecular Pattern ◽  
Compatible Interactions

Pathogens induce pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI) in plants. PAMPs are microbial molecules recognized by host plants as nonself signals, whereas pathogen effectors are evolved to aid in parasitism but are sometimes recognized by specific intracellular resistance proteins. In the absence of detectable ETI determining classical incompatible interactions, basal resistance exists during compatible and nonhost interactions. What triggers the basal resistance has remained elusive. Here, we provide evidence that ETI contributes to basal resistance during both compatible and nonhost Arabidopsis–Pseudomonas syringae interactions. Mutations in RAR1 and NDR1, two genes required for ETI, compromise basal resistance in both compatible and nonhost interactions. Complete nonhost resistance to P. syringae pv. tabaci required a functional type III secretion system. PTI appears to play a greater role in nonhost resistance than basal resistance during compatible interactions, because abrogation of PTI compromises basal resistance during nonhost but not compatible interactions. Strikingly, simultaneous abrogation of ETI and flagellin-induced PTI rendered plants completely susceptible to the nonadapted bacterium P. syringae pv. tabaci, indicating that ETI and PTI act synergistically during nonhost resistance. Thus, both nonhost resistance and basal resistance to virulent bacteria can be unified under PTI and ETI.

scholarly journals The Effect of Transcription Factor MYB14 on Defense Mechanisms in Vitis quinquangularis-Pingyi

2020 ◽  
Vol 21 (3) ◽  
pp. 706 ◽  
Author(s):  
Yangyang Luo ◽  
Qingyang Wang ◽  
Ru Bai ◽  
Ruixiang Li ◽  
Lu Chen ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Nicotiana Benthamiana ◽  
Defense Mechanisms ◽  
Qualitative Difference ◽  
Defense Responses ◽  
Molecular Pattern ◽  
Effector Triggered Immunity ◽  
Pathogen Associated Molecular Pattern ◽  
Basal Immunity ◽  
Stilbene Biosynthesis

In the current study, we identified a transcription factor, MYB14, from Chinese wild grape, Vitis quinquangularis-Pingyi (V. quinquangularis-PY), which could enhance the main stilbene contents and expression of stilbene biosynthesis genes (StSy/RS) by overexpression of VqMYB14. The promoter of VqMYB14 (pVqMYB14) was shown to be induced as part of both basal immunity (also called pathogen-associated molecular pattern (PAMP)-triggered immunity, PTI) and effector-triggered immunity (ETI), triggered by the elicitors flg22 and harpin, respectively. This was demonstrated by expression of pVqMYB14 in Nicotiana benthamiana and Vitis. We identified sequence differences, notably an 11 bp segment in pVqMYB14 that is important for the PTI/ETI, and particularly for the harpin-induced ETI response. In addition, we showed that activation of the MYB14 promoter correlates with differences in the expression of MYB14 and stilbene pattern induced by flg22 and harpin. An experimental model of upstream signaling in V. quinquangularis-PY is presented, where early defense responses triggered by flg22 and harpin partially overlap, but where the timing and levels differ. This translates into a qualitative difference with respect to patterns of stilbene accumulation.

scholarly journals The Majority of the Type III Effector Inventory of Pseudomonas syringae pv. tomato DC3000 Can Suppress Plant Immunity

2009 ◽  
Vol 22 (9) ◽  
pp. 1069-1080 ◽  
Author(s):  
Ming Guo ◽  
Fang Tian ◽  
Yashitola Wamboldt ◽  
James R. Alfano
Keyword(s):  
Pseudomonas Syringae ◽  
Plant Immunity ◽  
In Planta ◽  
Tomato Dc3000 ◽  
Type Iii Effector ◽  
Type Iii Effectors ◽  
Type Iii ◽  
Molecular Pattern ◽  
Effector Triggered Immunity ◽  
Type Iii Protein Secretion

The Pseudomonas syringae type III protein secretion system (T3SS) and the type III effectors it injects into plant cells are required for plant pathogenicity and the ability to elicit a hypersensitive response (HR). The HR is a programmed cell death that is associated with effector-triggered immunity (ETI). A primary function of P. syringae type III effectors appears to be the suppression of ETI and pathogen-associated molecular pattern–triggered immunity (PTI), which is induced by conserved molecules on microorganisms. We reported that seven type III effectors from P. syringae pv. tomato DC3000 were capable of suppressing an HR induced by P. fluorescens(pHIR11) and have now tested 35 DC3000 type III effectors in this assay, finding that the majority of them can suppress the HR induced by HopA1. One newly identified type III effector with particularly strong HR suppression activity was HopS2. We used the pHIR11 derivative pLN1965, which lacks hopA1, in related assays and found that a subset of the type III effectors that suppressed HopA1-induced ETI also suppressed an ETI response induced by AvrRpm1 in Arabidopsis thaliana. A. thaliana plants expressing either HopAO1 or HopF2, two type III effectors that suppressed the HopA1-induced HR, were reduced in the flagellin-induced PTI response as well as PTI induced by other PAMPs and allowed enhanced in planta growth of P. syringae. Collectively, our results suggest that the majority of DC3000 type III effectors can suppress plant immunity. Additionally, the construct pLN1965 will likely be a useful tool in determining whether other type III effectors or effectors from other types of pathogens can suppress either ETI, PTI, or both.

scholarly journals Revealing Differentially Expressed Genes and Identifying Effector Proteins of Puccinia striiformis f. sp. tritici in Response to High-Temperature Seedling Plant Resistance of Wheat Based on Transcriptome Sequencing

mSphere ◽  
2020 ◽  
Vol 5 (3) ◽  
Author(s):  
Fei Tao ◽  
Yangshan Hu ◽  
Chang Su ◽  
Juan Li ◽  
Lili Guo ◽  
...  
Keyword(s):  
High Temperature ◽  
Differentially Expressed Genes ◽  
Puccinia Striiformis ◽  
Effector Proteins ◽  
Differentially Expressed ◽  
Content Type ◽  
Molecular Pattern ◽  
Seedling Plant ◽  
Effector Triggered Immunity ◽  
Pathogen Associated Molecular Pattern

ABSTRACT Stripe rust, caused by Puccinia striiformis f. sp. tritici (Pst), is one of the most important diseases of wheat (Triticum aestivum L.) globally. Recently, more aggressive Pst races have evolved to acquire new virulence profiles and are adapted better to high temperature than most of the previous races. Breeding cultivars with durable high-temperature seedling-plant (HTSP) resistance is an important strategy for controlling stripe rust. Understanding the mechanism of wheat HTSP resistance against Pst is important for more efficient breeding to improve host resistance. In the present study, transcriptomic analysis identified 25 Pst differentially expressed genes (DEGs) that were involved in the HTSP resistance in wheat cultivar Xiaoyan6 (XY6). Functional annotation indicated that these DEGs are related to membrane proteins, mRNA binding proteins, cell membrane transporters, and synthesis of cell nitrogen compounds. Among these DEGs, a candidate effector, PstCEP1 (PSTG_13342), was identified and cloned, and its function was verified. Barley stripe mosaic virus (BSMV)-mediated host-induced gene silencing (HIGS) of PstCEP1 reduced Pst virulence. Signal peptide verification and functional testing in Nicotiana benthamiana indicated that PstCEP1 is a secreted protein and has the function of suppressing programmed cell death (PCD). PstCEP1 as a candidate effector was further supported by type three secretion system (TTSS)-mediated overexpression responding to wheat HTSP resistance via affecting the pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI). IMPORTANCE In the present study, we performed transcriptomic analysis to identify differentially expressed genes and effector proteins of Puccinia striiformis f. sp. tritici (Pst) in response to the high-temperature seedling-plant (HTSP) resistance in wheat. Experimental validation confirmed the function of the highest upregulated effector protein, PstCEP1. This study provides a key resource for understanding the biology and molecular basis of Pst responses to wheat HTSP resistance, and PstCEP1 may be used in future studies to understand pathogen-associated molecular pattern-triggered immunity and effector-triggered immunity processes in the Pst-wheat interaction system.

scholarly journals Basal Resistance Against Pseudomonas syringae in Arabidopsis Involves WRKY53 and a Protein with Homology to a Nematode Resistance Protein

2007 ◽  
Vol 20 (11) ◽  
pp. 1431-1438 ◽  
Author(s):  
Shane L. Murray ◽  
Robert A. Ingle ◽  
Lindsay N. Petersen ◽  
Katherine J. Denby
Keyword(s):  
Pseudomonas Syringae ◽  
Bacterial Pathogen ◽  
Nematode Resistance ◽  
Host Recognition ◽  
In Planta ◽  
Basal Resistance ◽  
Pathogen Effectors ◽  
Positive Regulators ◽  
Resistance Protein ◽  
Molecular Patterns

Basal resistance is the ultimately unsuccessful plant defense response to infection with a virulent pathogen. It is thought to be triggered by host recognition of pathogen-associated molecular patterns, with subsequent suppression of particular components by pathogen effectors. To identify novel components of Arabidopsis basal resistance against the bacterial pathogen Pseudomonas syringae pv. tomato, microarray expression profiling was carried out on the cir1 mutant, which displays enhanced resistance against P. syringae pv. tomato. This identified two genes, At4g23810 and At2g40000, encoding the transcription factor WRKY53 and the nematode resistance protein-like HSPRO2, whose expression was upregulated in cir1 prior to pathogen infection and in wild-type plants after P. syringae pv. tomato infection. WRKY53 and HSPRO2 are positive regulators of basal resistance. Knockout mutants of both genes were more susceptible to P. syringae pv. tomato infection than complemented lines, with increased growth of the pathogen in planta. WRKY53 and HSPRO2 appear to function downstream of salicylic acid and to be negatively regulated by signaling through jasmonic acid and ethylene.

scholarly journals Recent Advances in Effector-Triggered Immunity in Plants: New Pieces in the Puzzle Create a Different Paradigm

2021 ◽  
Vol 22 (9) ◽  
pp. 4709
Author(s):  
Quang-Minh Nguyen ◽  
Arya Bagus Boedi Iswanto ◽  
Geon Hui Son ◽  
Sang Hee Kim
Keyword(s):  
Host Plants ◽  
Crop Protection ◽  
Innate Immune ◽  
Leucine Rich Repeat ◽  
Resistance Proteins ◽  
Pathogen Effectors ◽  
Innate Immune Signaling ◽  
Current Perspective ◽  
Effector Triggered Immunity ◽  
Effector Recognition

Plants rely on multiple immune systems to protect themselves from pathogens. When pattern-triggered immunity (PTI)—the first layer of the immune response—is no longer effective as a result of pathogenic effectors, effector-triggered immunity (ETI) often provides resistance. In ETI, host plants directly or indirectly perceive pathogen effectors via resistance proteins and launch a more robust and rapid defense response. Resistance proteins are typically found in the form of nucleotide-binding and leucine-rich-repeat-containing receptors (NLRs). Upon effector recognition, an NLR undergoes structural change and associates with other NLRs. The dimerization or oligomerization of NLRs signals to downstream components, activates “helper” NLRs, and culminates in the ETI response. Originally, PTI was thought to contribute little to ETI. However, most recent studies revealed crosstalk and cooperation between ETI and PTI. Here, we summarize recent advancements in our understanding of the ETI response and its components, as well as how these components cooperate in the innate immune signaling pathways. Based on up-to-date accumulated knowledge, this review provides our current perspective of potential engineering strategies for crop protection.

scholarly journals GmRAR1 and GmSGT1 Are Required for Basal, R Gene–Mediated and Systemic Acquired Resistance in Soybean

2009 ◽  
Vol 22 (1) ◽  
pp. 86-95 ◽  
Author(s):  
Da-Qi Fu ◽  
Said Ghabrial ◽  
Aardra Kachroo
Keyword(s):  
Pseudomonas Syringae ◽  
Systemic Acquired Resistance ◽  
Soybean Mosaic Virus ◽  
Acquired Resistance ◽  
Bacterial Pathogen ◽  
R Gene ◽  
Extreme Resistance ◽  
Basal Resistance ◽  
Effector Triggered Immunity ◽  
Specific Proteins

RAR1, SGT1, and HSP90 are important components of effector-triggered immunity (ETI) in diverse plants, where RAR1 and SGT1 are thought to serve as HSP90 co-chaperones. We show that ETI in soybean requires RAR1 and SGT1 but not HSP90. Rsv1-mediated extreme resistance to Soybean mosaic virus (SMV) and Rpg-1b-mediated resistance to Pseudomonas syringae were compromised in plants silenced for GmRAR1 and GmSGT1-2 but not GmHSP90. This suggests that RAR1- or SGT1-dependant signaling is not always associated with a dependence on HSP90. Unlike in Arabidopsis, SGT1 in soybean also mediates ETI against the bacterial pathogen P. syringae. Similar to Arabidopsis, soybean RAR1 and SGT1 proteins interact with each other and two related HSP90 proteins. Plants silenced for GmHSP90 genes or GmRAR1 exhibited altered morphology, suggesting that these proteins also contribute to developmental processes. Silencing GmRAR1 and GmSGT1-2 impaired resistance to virulent bacteria and systemic acquired resistance (SAR) in soybean as well. Because the Arabidopsis rar1 mutant also showed a defect in SAR, we conclude that RAR1 and SGT1 serve as a point of convergence for basal resistance, ETI, and SAR. We demonstrate that, although soybean defense signaling pathways recruit structurally conserved components, they have distinct requirements for specific proteins.

MeBIK1, a novel cassava receptor-like cytoplasmic kinase, regulates PTI response of transgenic Arabidopsis

2018 ◽  
Vol 45 (6) ◽  
pp. 658
Author(s):  
Ke Li ◽  
Xi Xiong ◽  
Shousong Zhu ◽  
Hualan Liao ◽  
Xiaorong Xiao ◽  
...  
Keyword(s):  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Transgenic Arabidopsis ◽  
Isolation And Identification ◽  
Kinase Gene ◽  
Cassava Bacterial Blight ◽  
Molecular Pattern ◽  
Pathogen Associated Molecular Pattern ◽  
Ros Burst

Cassava bacterial blight is the most destructive disease in cassava, causing a significant reduction in its production. The innate immunity response, which has a broad spectrum and a persistent effect, is the basal defence of plants in response to pathogens. Isolation and identification of innate immune-related genes in cassava will contribute to understanding the disease resistance mechanism. In Arabidopsis, the receptor-like cytoplasmic kinase (RLCK) AtBIK1 is known to be an important signal mediator in pathogen-associated molecular pattern-triggered immunity (PTI) response, forming a signal complex from various receptors including the flagellin receptor FLS2, the chitin receptor CERK1 and the receptor for bacterial EF-Tu EFR (Zhang et al. 2010). In the present study, we selected a candidate receptor-like cytoplasmic kinase gene, MeBIK1, from the cassava genome. MeBIK1 encodes a 409 amino acid polypeptide comprising a typical serine/threonine protein kinase domain, and is located on the cell membrane. MeBIK1 gene expression was significantly increased upon stimulation with flagellin (flg22) and peaked at 1 h. In vitro genetic complementation experiment showed that MeBIK1 complemented the reduced pathogen-associated molecular pattern-triggered immunity (PTI) response in Arabidopsis bik1 mutant. Arabidopsis MeBIK1 overexpression lines OX1 demonstrated a strong resistance to Xanthomonas axonopodis pv. manihotis HN01, whereas its sensitivity to Pseudomonas syringae pv. tomato DC3000 was enhanced. The peak level of reactive oxygen species (ROS) burst was reached in different Arabidopsis plants (bik1, OX1 and wild type) at 12 min after induction with flg22. However, the OX1 showed significantly higher ROS levels than the control and mutant, whereas the lowest level of ROS burst was found in the bik1 mutant. These results indicate that cassava MeBIK1 has a similar function as Arabidopsis AtBIK1 and improves disease resistance in transgenic Arabidopsis by regulating the PTI response.

scholarly journals Novel Extracellular Chitinases Rapidly and Specifically Induced by General Bacterial Elicitors and Suppressed by Virulent Bacteria as a Marker of Early Basal Resistance in Tobacco

2006 ◽  
Vol 19 (2) ◽  
pp. 161-172 ◽  
Author(s):  
Péter G. Ott ◽  
Gabriella J. Varga ◽  
Ágnes Szatmári ◽  
Zoltán Bozsó ◽  
Éva Klement ◽  
...  
Keyword(s):  
Pseudomonas Syringae ◽  
Type Iii Secretion ◽  
Pathogenic Bacteria ◽  
Plant Cells ◽  
Basal Resistance ◽  
Living Plant ◽  
Bactericidal Efficacy ◽  
Environmental Light ◽  
Pathogenesis Related ◽  
Related Proteins

Early basal resistance (EBR, formerly known as early induced resistance) is triggered by general bacterial elicitors. EBR has been suggested to inhibit or retard expression of the type III secretion system of pathogenic bacteria and may also prevent nonpathogenic bacteria from colonizing the plant tissue. The quickness of EBR here plays a crucial role, compensating for a low bactericidal efficacy. This inhibitory activity should take place in the cell wall, as bacteria do not enter living plant cells. We found several soluble proteins in the intercellular fluid of tobacco leaf parenchyma that coincided with EBR under different environmental (light and temperature) conditions known to affect EBR. The two most prominent proteins proved to be novel chitinases (EC 3.2.1.14) that were transcriptionally induced before and during EBR development. Their expression in the apoplast was fast and not stress-regulated as opposed to many pathogenesis-related proteins. Nonpathogenic, saprophytic, and avirulent bacteria all induced EBR and the chitinases. Studies using these chitinases as EBR markers revealed that the virulent Pseudomonas syringae pv. tabaci, being sensitive to EBR, must suppress it while suppressing the chitinases. EBR, the chitinases, as well as their suppression are quantitatively related, implying a delicate balance determining the outcome of an infection.

Sign in / Sign up

Export Citation Format

Share Document