Infection of tobacco with different Pseudomonas syringae pathovars leads to distinct morphotypes of programmed cell death

ABSTRACT AvrPtoB is a type III effector protein from Pseudomonas syringae pv. tomato that physically interacts with the tomato Pto kinase and, depending on the host genotype, either elicits or suppresses programmed cell death associated with plant immunity. We reported previously that avrPtoB-related sequences are present in diverse gram-negative phytopathogenic bacteria. Here we describe characterization of avrPtoB homologs from P. syringae pv. tomato T1, PT23, and JL1065, P. syringae pv. syringae B728a, and P. syringae pv. maculicola ES4326. The avrPtoB homolog from P. syringae pv. maculicola, hopPmaL, was identified previously. The four new genes identified in this study are designated avrPtoBT1 , avrPtoBPT23 , avrPtoBJL1065 , and avrPtoBB728a . The AvrPtoB homologs exhibit 52 to 66% amino acid identity with AvrPtoB. Transcripts of each of the avrPtoB homologs were detected in the Pseudomonas strains from which they were isolated. Proteins encoded by the homologs were detected in all strains except P. syringae pv. tomato T1, suggesting that T1 suppresses accumulation of AvrPtoBT1. All of the homologs interacted with the Pto kinase in a yeast two-hybrid system and elicited a Pto-dependent defense response when they were delivered into leaf cells by DC3000ΔavrPtoΔavrPtoB, a P. syringae pv. tomato strain with a deletion of both avrPto and avrPtoB. Like AvrPtoB, all of the homologs enhanced the ability of DC3000ΔavrPtoΔavrPtoB to form lesions on leaves of two susceptible tomato lines. With the exception of HopPmaL which lacks the C-terminal domain, all AvrPtoB homologs suppressed programmed cell death elicited by the AvrPto-Pto interaction in an Agrobacterium-mediated transient assay. Thus, despite their divergent sequences, AvrPtoB homologs from diverse P. syringae pathovars have conserved avirulence and virulence activities similar to AvrPtoB activity.

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Harpin Inactivates Mitochondria in Arabidopsis Suspension Cells

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi.2004.17.2.131 ◽

2004 ◽

Vol 17 (2) ◽

pp. 131-139 ◽

Cited By ~ 115

Author(s):

Maren Krause ◽

Jörg Durner

Keyword(s):

Cell Death ◽

Programmed Cell Death ◽

Pseudomonas Syringae ◽

Stress Responses ◽

Time Course ◽

Defense Responses ◽

Ros Generation ◽

Suspension Cells ◽

Mitochondrial Functions ◽

Arabidopsis Cells

Harpin is a well-known proteinaceous bacterial elicitor that can induce an oxidative burst and programmed cell death in various host plants. Given the demonstrated roles of mitochondria in animal apoptosis, we investigated the effect of harpin from Pseudomonas syringae on mitochondrial functions in Arabidopsis suspension cells in detail. Fluorescence microscopy in conjunction with double-staining for reactive oxygen species (ROS) and mitochondria suggested co-localization of mitochondria and ROS generation. Plant defense responses or cell death after pathogen attack have been suggested to be regulated by the concerted action of ROS and nitric oxide (NO). However, although Arabidopsis cells respond to harpin treatment with NO generation, time course analyses suggest that NO generation is not involved in initial responses but, rather, is a consequence of cellular decay. Among the fast responses we observed was a decrease of the mitochondrial membrane potential Δψm and, possibly as a direct consequence, of ATP production. Furthermore, treatment of Arabidopsis cells with harpin protein induced a rapid cytochrome C release from mitochondria into the cytosol, which is regarded as a hallmark of programmed cell death or apoptosis. Northern and DNA array analyses showed strong induction of protecting or scavenging systems such as alternative oxidase and small heat shock proteins, components that are known to be associated with cellular stress responses. In sum, the presented data suggest that harpin inactivates mitochondria in Arabidopsis cells.

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Modulation of chloroplast components and defense responses during programmed cell death in tobacco infected with Pseudomonas syringae

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2020.05.086 ◽

2020 ◽

Vol 528 (4) ◽

pp. 753-759

Author(s):

Bao Quoc Tran ◽

Sunyo Jung

Keyword(s):

Cell Death ◽

Programmed Cell Death ◽

Pseudomonas Syringae ◽

Defense Responses

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

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi.2004.17.12.1328 ◽

2004 ◽

Vol 17 (12) ◽

pp. 1328-1336 ◽

Cited By ~ 25

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.

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