Pseudomonas syringae Effector Protein AvrB Perturbs Arabidopsis Hormone Signaling by Activating MAP Kinase 4 (original) (raw)
Related papers
A Pseudomonas syringae Effector Inactivates MAPKs to Suppress PAMP-Induced Immunity in Plants
Cell Host & Microbe, 2007
Pathogen-associated molecular patterns (PAMPs) elicit basal defense responses in plants, and, in turn, pathogens have evolved mechanisms to overcome these PAMP-induced defenses. To suppress immunity, the phytopathogenic bacterium Pseudomonas syringae secretes effector proteins, the biochemical function and virulence targets of which remain largely unknown. We show that HopAI1, an effector widely conserved in both plant and animal bacterial pathogens, inhibits the Arabidopsis mitogen-activated protein kinases (MAPKs) activated by exposure to PAMPs. HopAI1 inactivates MAPKs by removing the phosphate group from phosphothreonine through a unique phosphothreonine lyase activity, which is required for HopAI1 function. The inhibition of MAPKs by HopA1 suppresses two independent downstream events, namely the reinforcement of cell wall defense and transcriptional activation of PAMP response genes. The MAPKs MPK3 and MPK6 physically interact with HopAI1 indicating that they are direct targets of HopAI1. These findings uncover a mechanism by which Pseudomonas syringae overcomes host innate immunity to promote pathogenesis.
New Phytologist, 2003
• The mechanisms by which plant growth-promoting rhizobacteria (PGPR) mediate induced systemic resistance are currently being intensively investigated from the viewpoint of signal transduction pathways within plants. • Here, we determined whether our well-characterized PGPR strains, which have demonstrated induced resistance on various plants, also elicit induced resistance in Arabidopsis thaliana. Nine different PGPR strains were evaluated for their capacity to cause induced resistance on Arabidopsis against two pathovars of Pseudomonas syringae. Six strains significantly reduced severity of P. syringae pv. tomato, whereas seven strains reduced severity of P. syringae pv. maculicola. • From the initial screenings, four strains (90-166, SE34, 89B61 and T4) were selected because of their consistent induced resistance capacity. Elicitation of induced resistance with these strains depended on how disease severity was measured. Three strains (90-166, 89B61 and T4) induced resistance in NahG plants (SA-deficient), indicating a salicylic acid-independent pathway, which agrees with the previously reported pathway for induced resistance by PGPR. However, differences from the reported pathway were noted with strain 89B61, which did not require jasmonic acid or ethylene signaling pathways for induced resistance, and with strain T4, which induced resistance in npr1 plants. • These results indicate that strains 89B61 and T4 induce resistance via a new pathway or possibly a variation of the previously reported pathway. This information will broaden our understanding of ways in which microorganisms can signal physiological changes in plants.
Pseudomonas syringae manipulates systemic plant defenses against pathogens and herbivores
Proceedings of The National Academy of Sciences, 2005
Many pathogens are virulent because they specifically interfere with host defense responses and therefore can proliferate. Here, we report that virulent strains of the bacterial phytopathogen Pseudomonas syringae induce systemic susceptibility to secondary P. syringae infection in the host plant Arabidopsis thaliana. This systemic induced susceptibility (SIS) is in direct contrast to the well studied avirulence͞R gene-dependent resistance response known as the hypersensitive response that elicits systemic acquired resistance. We show that P. syringae-elicited SIS is caused by the production of coronatine (COR), a pathogen-derived functional and structural mimic of the phytohormone jasmonic acid (JA). These data suggest that SIS may be a consequence of the previously described mutually antagonistic interaction between the salicylic acid and JA signaling pathways. Virulent P. syringae also has the potential to induce net systemic susceptibility to herbivory by an insect (Trichoplusia ni, cabbage looper), but this susceptibility is not caused by COR. Rather, consistent with its role as a JA mimic, COR induces systemic resistance to T. ni. These data highlight the complexity of defense signaling interactions among plants, pathogens, and herbivores.
Phytopathology Research, 2022
Phytohormones play an essential role in plant immune responses. Many phytopathogens secret effector proteins to promote infection and plant hormone signaling pathways are considered to be the potential targets of effectors. Here we found that abscisic acid (ABA) signaling was activated rapidly upon infection with Pseudomonas syringae pv. tomato (Pst). Pst secretes the effector AvrPtoB to target ABA 8′-hydroxylase CYP707As for degradation in Arabidopsis thaliana. CYP707As hydroxylate ABA to an inactive form. The degradation of CYP707As resulted in ABA accumulation and compromised plant immune responses. Our study demonstrated that Pst could hijack the key components of Arabidopsis ABA signaling pathway to cause disease.
Proceedings of the National Academy of Sciences, 2014
Significance Pathogenic bacteria inject effector proteins into the host to suppress its defenses. However, bacteria produce the effector proteins and injection machinery only upon recognition of a potential host. Here we identified an Arabidopsis mutant, mapk phosphatase 1 ( mkp1 ), with decreased levels of chemical signals recognized by the bacterium, thus making the plant more resistant by suppressing the ability of the pathogen, Pseudomonas syringae , to express and inject effector proteins. Reapplying these chemical signals not only eliminated resistance in the mkp1 mutant but also suppressed resistance in wild-type plants with a preinduced immune response. These results demonstrate an important layer in determining the biological outcome during host–pathogen interactions and may provide new targets for enhancing resistance against bacterial pathogens.
PLoS ONE, 2013
Pseudomonas syringae pv tomato strain DC3000 (Pto) delivers several effector proteins promoting virulence, including HopM1, into plant cells via type III secretion. HopM1 contributes to full virulence of Pto by inducing degradation of Arabidopsis proteins, including AtMIN7, an ADP ribosylation factor-guanine nucleotide exchange factor. Pseudomonas syringae pv phaseolicola strain NPS3121 (Pph) lacks a functional HopM1 and elicits robust defenses in Arabidopsis thaliana, including accumulation of pathogenesis related 1 (PR-1) protein and deposition of callose-containing cell wall fortifications. We have examined the effects of heterologously expressed HopM1 Pto on Pph-induced defenses. HopM1 suppresses Pphinduced PR-1 expression, a widely used marker for salicylic acid (SA) signaling and systemic acquired resistance. Surprisingly, HopM1 reduces PR-1 expression without affecting SA accumulation and also suppresses the low levels of PR-1 expression apparent in SA-signaling deficient plants. Further, HopM1 enhances the growth of Pto in SA-signaling deficient plants. AtMIN7 contributes to Pph-induced PR-1 expression. However, HopM1 fails to degrade AtMIN7 during Pph infection and suppresses Pph-induced PR-1 expression and callose deposition in wild-type and atmin7 plants. We also show that the HopM1-mediated suppression of PR-1 expression is not observed in plants lacking the TGA transcription factor, TGA3. Our data indicate that HopM1 promotes bacterial virulence independent of suppressing SA-signaling and links TGA3, AtMIN7, and other HopM1 targets to pathways distinct from the canonical SA-signaling pathway contributing to PR-1 expression and callose deposition. Thus, efforts to understand this key effector must consider multiple targets and unexpected outputs of its action.
Arabidopsis MAPKKK δ-1 is required for full immunity against bacterial and fungal infection
Journal of Experimental Botany, 2019
The genome of Arabidopsis encodes more than 60 mitogen-activated protein kinase kinase (MAPKK) kinases (MAPKKKs); however, the functions of most MAPKKKs and their downstream MAPKKs are largely unknown. Here, MAPKKK δ-1 (MKD1), a novel Raf-like MAPKKK, was isolated from Arabidopsis as a subunit of a complex including the transcription factor AtNFXL1, which is involved in the trichothecene phytotoxin response and in disease resistance against the bacterial pathogen Pseudomonas syringae pv. tomato DC3000 (PstDC3000). A MKD1-dependent cascade positively regulates disease resistance against PstDC3000 and the trichothecene mycotoxin-producing fungal pathogen Fusarium sporotrichioides. MKD1 expression was induced by trichothecenes derived from Fusarium species. MKD1 directly interacted with MKK1 and MKK5 in vivo, and phosphorylated MKK1 and MKK5 in vitro. Correspondingly, mkk1 mutants and MKK5RNAi transgenic plants showed enhanced susceptibility to F. sporotrichioides. MKD1 was required fo...
Cell Host & Microbe, 2010
Cell-surface-localized plant immune receptors, such as FLS2, detect pathogen-associated molecular patterns (PAMPs) and initiate PAMP-triggered immunity (PTI) through poorly understood signal-transduction pathways. The pathogenic Pseudomonas syringae effector AvrPphB, a cysteine protease, cleaves the Arabidopsis receptor-like cytoplasmic kinase PBS1 to trigger cytoplasmic immune receptor RPS5-specified effector-triggered immunity (ETI). Analyzing the function of AvrPphB in plants lacking RPS5, we find that AvrPphB can inhibit PTI by cleaving additional PBS1-like (PBL) kinases, including BIK1, PBL1, and PBL2. In unstimulated plants, BIK1 and PBL1 interact with FLS2 and are rapidly phosphorylated upon FLS2 activation by its ligand flg22. Genetic and molecular analyses indicate that BIK1, and possibly PBL1, PBL2, and PBS1, integrate immune signaling from multiple immune receptors. Whereas AvrPphB-mediated degradation of one of these kinases, PBS1, is monitored by RPS5 to initiate ETI, this pathogenic effector targets other PBL kinases for PTI inhibition.
Plant physiology, 2015
Many bacterial pathogens of plants and animals deliver effector proteins into host cells to promote infection. Elucidation of how pathogen effector proteins function not only is critical for understanding bacterial pathogenesis, but also provides a useful tool in discovering the functions of host genes. In this study, we characterized the Pseudomonas syringae pv. tomato DC3000 effector protein AvrE, the founding member of a widely distributed, yet functionally enigmatic, bacterial effector family. We show that AvrE is localized in the plasma membrane (PM) and PM-associated vesicle-like structures in the plant cell. AvrE contains two physically interacting domains, and the N-terminal portion contains a PM-localization signal. Genome-wide microarray analysis indicates that AvrE, as well as a functionally-redundant effector HopM1, down-regulates the expression of the NDR1/HIN1-Like 13 gene in Arabidopsis. Mutational analysis shows that NHL13 is required for plant immunity, as the nhl13...
Molecular Plant-Microbe Interactions®, 2006
Many plant pathogens suppress antimicrobial defenses using virulence factors that modulate endogenous host defenses. The Pseudomonas syringae phytotoxin coronatine (COR) is believed to promote virulence by acting as a jasmonate analog, because COR-insensitive 1 (coi1) Arabidopsis thaliana and tomato mutants are impaired in jasmonate signaling and exhibit reduced susceptibility to P. syringae. To further investigate the role of jasmonate signaling in disease development, we analyzed several jasmonate-insensitive A. thaliana mutants for susceptibility to P. syringae pv. tomato strain DC3000 and sensitivity to COR. Jasmonate-insensitive1 (jin1) mutants exhibit both reduced susceptibility to P. syringae pv. tomato DC3000 and reduced sensitivity to COR, whereas jasmonate-resistant 1 (jar1) plants exhibit wild-type responses to both COR and P. syringae pv. tomato DC3000. A jin1 jar1 double mutant does not exhibit enhanced jasmonate insensitivity, suggesting that JIN1 functions downstream ...