scholarly journals Erwinia amylovora Type Three–Secreted Proteins Trigger Cell Death and Defense Responses in Arabidopsis thaliana

2008 ◽  
Vol 21 (8) ◽  
pp. 1076-1086 ◽  
Author(s):  
A. Degrave ◽  
M. Fagard ◽  
C. Perino ◽  
M. N. Brisset ◽  
S. Gaubert ◽  
...  

Erwinia amylovora is the bacterium responsible for fire blight, a necrotic disease affecting plants of the rosaceous family. E. amylovora pathogenicity requires a functional type three secretion system (T3SS). We show here that E. amylovora triggers a T3SS-dependent cell death on Arabidopsis thaliana. The plants respond by inducing T3SS-dependent defense responses, including salicylic acid (SA)-independent callose deposition, activation of the SA defense pathway, reactive oxygen species (ROS) accumulation, and part of the jasmonic acid/ethylene defense pathway. Several of these reactions are similar to what is observed in host plants. We show that the cell death triggered by E. amylovora on A. thaliana could not be simply explained by the recognition of AvrRpt2ea by the resistance gene product RPS2. We then analyzed the role of type three-secreted proteins (T3SPs) DspA/E, HrpN, and HrpW in the induction of cell death and defense reactions in A. thaliana following infection with the corresponding E. amylovora mutant strains. HrpN and DspA/E were found to play an important role in the induction of cell death, activation of defense pathways, and ROS accumulation. None of the T3SPs tested played a major role in the induction of SA-independent callose deposition. The relative importance of T3SPs in A. thaliana is correlated with their relative importance in the disease process on host plants, indicating that A. thaliana can be used as a model to study their role.

2006 ◽  
Vol 19 (1) ◽  
pp. 16-24 ◽  
Author(s):  
Tristan Boureau ◽  
Hayat ElMaarouf-Bouteau ◽  
Amélie Garnier ◽  
Marie-Noëlle Brisset ◽  
Claude Perino ◽  
...  

Erwinia amylovora is responsible for fire blight, a necrotic disease of apples and pears. E. amylovora relies on a type III secretion system (TTSS) to induce disease on hosts and hypersensitive response (HR) on nonhost plants. The DspA/E protein is essential for E. amylovora pathogenicity and is secreted via the TTSS in vitro. DspA/E belongs to a type III effector family that is conserved in several phytopathogenic bacteria. In E. amylovora, DspA/E has been implicated in the generation of an oxidative stress during disease and the suppression of callose deposition. We investigated the fate of DspA/E in planta. DspA/E delivered artificially to apple or tobacco cells by agroinfection induced necrotic symptoms, indicating that DspA/E was probably injected via the TTSS. We confirmed that DspA/E acts as a major cell-death inducer during disease and HR, because the dspA/E mutant is severely impaired in its ability to induce electrolyte leakage in apple and tobacco leaves. Expression of the defense marker gene PR1 was delayed when dspA/E was transiently expressed in tobacco, suggesting that DspA/E-mediated necrosis may be associated with an alteration of defense responses.


2018 ◽  
Vol 31 (3) ◽  
pp. 311-322 ◽  
Author(s):  
Shune Wang ◽  
Ying Zheng ◽  
Chun Gu ◽  
Chan He ◽  
Mengying Yang ◽  
...  

Bacillus cereus AR156 (AR156) is a plant growth–promoting rhizobacterium capable of inducing systemic resistance to Pseudomonas syringae pv. tomato in Arabidopsis thaliana. Here, we show that, when applied to Arabidopsis leaves, AR156 acted similarly to flg22, a typical pathogen-associated molecular pattern (PAMP), in initiating PAMP-triggered immunity (PTI). AR156-elicited PTI responses included phosphorylation of MPK3 and MPK6, induction of the expression of defense-related genes PR1, FRK1, WRKY22, and WRKY29, production of reactive oxygen species, and callose deposition. Pretreatment with AR156 still significantly reduced P. syringae pv. tomato multiplication and disease severity in NahG transgenic plants and mutants sid2-2, jar1, etr1, ein2, npr1, and fls2. This suggests that AR156-induced PTI responses require neither salicylic acid, jasmonic acid, and ethylene signaling nor flagella receptor kinase FLS2, the receptor of flg22. On the other hand, AR156 and flg22 acted in concert to differentially regulate a number of AGO1-bound microRNAs that function to mediate PTI. A full-genome transcriptional profiling analysis indicated that AR156 and flg22 activated similar transcriptional programs, coregulating the expression of 117 genes; their concerted regulation of 16 genes was confirmed by real-time quantitative polymerase chain reaction analysis. These results suggest that AR156 activates basal defense responses to P. syringae pv. tomato in Arabidopsis, similarly to flg22.


2012 ◽  
Vol 25 (3) ◽  
pp. 421-430 ◽  
Author(s):  
Manon Moreau ◽  
Alexandre Degrave ◽  
Régine Vedel ◽  
Frédérique Bitton ◽  
Oriane Patrit ◽  
...  

Erwinia amylovora causes fire blight in rosaceous plants. In nonhost Arabidopsis thaliana, E. amylovora triggers necrotic symptoms associated with transient bacterial multiplication, suggesting either that A. thaliana lacks a susceptibility factor or that it actively restricts E. amylovora growth. Inhibiting plant protein synthesis at the time of infection led to an increase in necrosis and bacterial multiplication and reduced callose deposition, indicating that A. thaliana requires active protein synthesis to restrict E. amylovora growth. Analysis of the callose synthase–deficient pmr4-1 mutant indicated that lack of callose deposition alone did not lead to increased sensitivity to E. amylovora. Transcriptome analysis revealed that approximately 20% of the genes induced following E. amylovora infection are related to defense and signaling. Analysis of mutants affected in NDR1 and EDS1, two main components of the defense-gene activation observed, revealed that E. amylovora multiplied ten times more in the eds1-2 mutant than in the wild type but not in the ndr1-1 mutant. Analysis of mutants affected in three WRKY transcription factors showing EDS1-dependent activation identified WRKY46 and WRKY54 as positive regulators and WRKY70 as a negative regulator of defense against E. amylovora. Altogether, we show that EDS1 is a positive regulator of nonhost resistance against E. amylovora in A. thaliana and hypothesize that it controls the production of several effective defenses against E. amylovora through the action of WRKY46 and WRKY54, while WRKY70 acts as a negative regulator.


2019 ◽  
Vol 20 (13) ◽  
pp. 3243 ◽  
Author(s):  
Yue Zhang ◽  
Qunen Liu ◽  
Yingxin Zhang ◽  
Yuyu Chen ◽  
Ning Yu ◽  
...  

Lesion mimic mutants are excellent models for research on molecular mechanisms of cell death and defense responses in rice. We identified a new rice lesion mimic mutant lmm24 from a mutant pool of indica rice cultivar “ZhongHui8015”. The LMM24 gene was identified by MutMap, and LMM24 was confirmed as a receptor-like cytoplasmic kinase 109 by amino acid sequence analysis. The lmm24 mutant displayed dark brown lesions in leaves and growth retardation that were not observed in wild-type ZH8015. The results of histochemical staining and TUNEL assays showed enhanced ROS accumulation and cell death in lmm24. Chloroplast degradation was observed in lmm24 leaves, with decreased expression of photosynthesis-related genes and increased expression of the senescence-induced STAYGREEN (SGR) gene and other senescence-associated genes. Furthermore, lmm24 exhibited enhanced resistance to rice blast fungus Magnaporthe oryzae (M. oryzae) and up-regulation of defense response genes. Our data demonstrate that LMM24 regulates cell death and defense responses in rice.


2007 ◽  
Vol 120 (18) ◽  
pp. 3271-3278 ◽  
Author(s):  
D. Reboutier ◽  
C. Frankart ◽  
J. Briand ◽  
B. Biligui ◽  
J.-P. Rona ◽  
...  

2015 ◽  
Vol 28 (8) ◽  
pp. 913-926 ◽  
Author(s):  
Ke-Chun Peng ◽  
Chao-Wen Wang ◽  
Chih-Hang Wu ◽  
Chun-Tzu Huang ◽  
Ruey-Fen Liou

During host-pathogen interactions, pattern recognition receptors form complexes with proteins, such as receptor-like kinases, to elicit pathogen-associated molecular pattern-triggered immunity (PTI), an evolutionarily conserved plant defense program. However, little is known about the components of the receptor complex, as are the molecular events leading to PTI induced by the oomycete Phytophthora pathogen. Here, we demonstrate that tomato (Solanum lycopersicum) SlSOBIR1 and SlSOBIR1-like genes are involved in defense responses to Phytophthora parasitica. Silencing of SlSOBIR1 and SlSOBIR1-like enhanced susceptibility to P. parasitica in tomato. Callose deposition, reactive oxygen species production, and PTI marker gene expression were compromised in SlSOBIR1- and SlSOBIR1-like–silenced plants. Interestingly, P. parasitica infection and elicitin (ParA1) treatment induced the relocalization of SlSOBIR1 from the plasma membrane to endosomal compartments and silencing of NbSOBIR1 compromised ParA1-mediated cell death on Nicotiana benthamiana. Moreover, the SlSOBIR1 kinase domain is indispensable for ParA1 to trigger SlSOBIR1 internalization and plant cell death. Taken together, these results support the idea of participation of solanaceous SOBIR1/EVR homologs in the perception of elicitins and indicate their important roles in plant basal defense against oomycete pathogens.


2019 ◽  
Vol 20 (20) ◽  
pp. 5032 ◽  
Author(s):  
Pingping Nie ◽  
Chen Chen ◽  
Qian Yin ◽  
Chunhao Jiang ◽  
Jianhua Guo ◽  
...  

Small RNAs function to regulate plant defense responses to pathogens. We previously showed that miR825 and miR825* downregulate Bacillus cereus AR156 (AR156)-triggered systemic resistance to Pseudomonassyringae pv. tomato DC3000 in Arabidopsis thaliana (Arabidopsis). Here, Northern blotting revealed that miR825 and miR825* were more strongly downregulated in wild type Arabidopsis Col-0 (Col-0) plants pretreated with AR156 than in nontreated plants upon Botrytis cinerea (B. cinerea) B1301 infection. Furthermore, compared with Col-0, transgenic plants with attenuated miR825 and miR825* expression were more resistant to B. cinerea B1301, yet miR825- and miR825*-overexpressing (OE) plants were more susceptible to the pathogen. With AR156 pretreatment, the transcription of four defense-related genes (PR1, PR2, PR5, and PDF1.2) and cellular defense responses (hydrogen peroxide production and callose deposition) were faster and stronger in miR825 and miR825* knockdown lines but weaker in their OE plants than in Col-0 plants upon pathogen attack. Also, AR156 pretreatment caused stronger phosphorylation of MPK3 and MPK6 and expression of FRK1 and WRKY53 genes upon B. cinerea B1301 inoculation in miR825 and miR825* knockdown plants than in Col-0 plants. Additionally, the assay of agrobacterium-mediated transient co-expression in Nicotiana benthamiana confirmed that AT5G40910, AT5G38850, AT3G04220, and AT5G44940 are target genes of miR825 or miR825*. Compared with Col-0, the target mutant lines showed higher susceptibility to B. cinerea B1301, while still expressing AR156-triggered induced systemic resistance (ISR). The two-way analysis of variance (ANOVA) revealed a significant (P < 0.01) interactive effect of treatment and genotype on the defense responses. Hence, miR825 and miR825*act as negative regulators of AR156-mediated systemic resistance to B. cinerea B1301 in Arabidopsis.


2006 ◽  
Vol 19 (5) ◽  
pp. 512-520 ◽  
Author(s):  
Takumi Nishiuchi ◽  
Daisuke Masuda ◽  
Hideo Nakashita ◽  
Kazuya Ichimura ◽  
Kazuo Shinozaki ◽  
...  

Phytopathogenic fungi such as Fusarium spp. synthesize trichothecene family phytotoxins. Although the type B trichothecene, deoxynivalenol (DON), is thought to be a virulence factor allowing infection of plants by their trichothecene-producing Fusarium spp., little is known about effects of trichothecenes on the defense response in host plants. Therefore, in this article, we investigated these effects of various trichothecenes in Fusarium-susceptible Arabidopsis thaliana. Necrotic lesions were observed in Arabidopsis leaves infiltrated by 1 μM type A trichothecenes such as T-2 toxin. Trichothecene-induced lesions exhibited dead cells, callose deposition, generation of hydrogen peroxide, and accumulation of salicylic acids. Moreover, infiltration by trichothecenes caused rapid and prolonged activation of two mitogen-activated protein kinases and induced expression of both PR-1 and PDF1.2 genes. Thus, type A trichothecenes trigger the cell death by activation of an elicitor-like signaling pathway in Arabidopsis. Although DON did not have such an activity even at 10 μM, translational inhibition by DON was observed at concentrations above 5 μM. These results suggested that DON is capable of inhibiting translation in Arabidopsis cells without induction of the elicitor-like signaling pathway.


2007 ◽  
Vol 20 (1) ◽  
pp. 31-40 ◽  
Author(s):  
Gopaljee Jha ◽  
Ramanan Rajeshwari ◽  
Ramesh V. Sonti

The type II (T2S) and type III (T3S) secretion systems are important for virulence of Xanthomonas oryzae pv. oryzae, causal agent of bacterial leaf blight of rice. The T3S of gram-negative bacterial plant pathogens has been shown to suppress host defense responses, including programmed cell death reactions, whereas the T2S is involved in secreting cell-wall-degrading enzymes. Here, we show that a T3S-deficient (T3S¯) mutant of X. oryzae pv. oryzae can induce a basal plant defense response seen as callose deposition, immunize rice against subsequent X. oryzae pv. oryzae infection, and cause cell-death-associated nuclear fragmentation. A T2S¯ T3S¯ double mutant exhibited a substantial reduction in the ability to evoke these responses. We purified two major effectors of the X. oryzae pv. oryzae T2S and characterized them to be a cellulase (ClsA) and a putative cellobiosidase (CbsA). The purified ClsA, CbsA, and lipase/esterase (LipA; a previously identified T2S effector) proteins induced rice defense responses that were suppressible by X. oryzae pv. oryzae in a T3S-dependent manner. These defense responses also were inducible by the products of the action of these purified proteins on rice cell walls. We further show that a CbsA¯ mutant or a ClsA¯ LipA¯ double mutant are severely virulence deficient. These results indicate that the X. oryzae pv. oryzae T2S secretes important virulence factors, which induce innate rice defense responses that are suppressed by T3S effectors to enable successful infection.


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