Type III effector proteins from the plant pathogen Xanthomonas and their role in the interaction with the host plant

2006 ◽  
Vol 163 (3) ◽  
pp. 233-255 ◽  
Author(s):  
Doreen Gürlebeck ◽  
Frank Thieme ◽  
Ulla Bonas
Keyword(s):  
Host Plant ◽  
Plant Pathogen ◽  
Effector Proteins ◽  
Type Iii Effector ◽  
Type Iii

scholarly journals The Pseudomonas syringae Type III Effector HopAM1 Enhances Virulence on Water-Stressed Plants

2008 ◽  
Vol 21 (3) ◽  
pp. 361-370 ◽  
Author(s):  
Ajay K. Goel ◽  
Derek Lundberg ◽  
Miguel A. Torres ◽  
Ryan Matthews ◽  
Chiharu Akimoto-Tomiyama ◽  
...  
Keyword(s):  
Host Plant ◽  
Pseudomonas Syringae ◽  
Stomatal Closure ◽  
Defense Responses ◽  
Effector Proteins ◽  
Host Cells ◽  
Type Iii Effector ◽  
Type Iii Effectors ◽  
Type Iii ◽  
Conditional Expression

Pseudomonas syringae strains deliver diverse type III effector proteins into host cells, where they can act as virulence factors. Although the functions of the majority of type III effectors are unknown, several have been shown to interfere with plant basal defense mechanisms. Type III effectors also could contribute to bacterial virulence by enhancing nutrient uptake and pathogen adaptation to the environment of the host plant. We demonstrate that the type III effector HopAM1 (formerly known as AvrPpiB) enhances the virulence of a weak pathogen in plants that are grown under drought stress. This is the first report of a type III effector that aids pathogen adaptation to water availability in the host plant. Expression of HopAM1 makes transgenic Ws-0 Arabidopsis hypersensitive to abscisic acid (ABA) for stomatal closure and germination arrest. Conditional expression of HopAM1 in Arabidopsis also suppresses basal defenses. ABA responses overlap with defense responses and ABA has been shown to suppress defense against P. syringae pathogens. We propose that HopAM1 aids P. syringae virulence by manipulation of ABA responses that suppress defense responses. In addition, host ABA responses enhanced by type III delivery of HopAM1 protect developing bacterial colonies inside leaves from osmotic stress.

Distribution of espI among clinical enterohaemorrhagic and enteropathogenic Escherichia coli isolates

2004 ◽  
Vol 53 (11) ◽  
pp. 1145-1149 ◽  
Author(s):  
Rosanna Mundy ◽  
Claire Jenkins ◽  
Jun Yu ◽  
Henry Smith ◽  
Gad Frankel
Keyword(s):  
Escherichia Coli ◽  
Type Iii Secretion ◽  
Severe Disease ◽  
Pathogenicity Island ◽  
Effector Proteins ◽  
Effector Protein ◽  
Enteropathogenic Escherichia Coli ◽  
Type Iii Effector ◽  
Type Iii

Enterohaemorrhagic (EHEC) and enteropathogenic (EPEC) Escherichia coli are important diarrhoeagenic pathogens; infection is dependent on translocation of a number of type III effector proteins. Until recently all the known effectors were encoded on the LEE pathogenicity island, which also encodes the adhesin intimin and the type III secretion apparatus. Recently, a novel non-LEE effector protein, EspI/NleA, which is required for full virulence in vivo and is encoded on a prophage, was identified. The aim of this study was to determine the distribution of espI among clinical EHEC and EPEC isolates. espI was detected in 86 % and 53 % of LEE+ EHEC and EPEC strains, respectively. Moreover, the espI gene was more commonly found in patients suffering from a more severe disease.

scholarly journals A Plant Pathogen Type III Effector Protein Subverts Translational Regulation to Boost Host Polyamine Levels

2019 ◽  
Vol 26 (5) ◽  
pp. 638-649.e5 ◽  
Author(s):  
Dousheng Wu ◽  
Edda von Roepenack-Lahaye ◽  
Matthias Buntru ◽  
Orlando de Lange ◽  
Niklas Schandry ◽  
...  
Keyword(s):  
Plant Pathogen ◽  
Translational Regulation ◽  
Effector Protein ◽  
Type Iii Effector ◽  
Type Iii

scholarly journals The Type III Effector NleD from Enteropathogenic Escherichia coli Differentiates between Host Substrates p38 and JNK

2016 ◽  
Vol 85 (2) ◽  
Author(s):  
Kristina Creuzburg ◽  
Cristina Giogha ◽  
Tania Wong Fok Lung ◽  
Nichollas E. Scott ◽  
Sabrina Mühlen ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Effector Proteins ◽  
Mitogen Activated Protein Kinase ◽  
Mass Spectrometry Analysis ◽  
Single Amino Acid ◽  
Luciferase Reporter ◽  
Type Iii Effector ◽  
Type Iii ◽  
Infected Cells

ABSTRACT Enteropathogenic Escherichia coli (EPEC) is a gastrointestinal pathogen that utilizes a type III secretion system (T3SS) to inject an array of virulence effector proteins into host enterocytes to subvert numerous cellular processes for successful colonization and dissemination. The T3SS effector NleD is a 26-kDa zinc metalloprotease that is translocated into host enterocytes, where it directly cleaves and inactivates the mitogen-activated protein kinase signaling proteins JNK and p38. Here a library of 91 random transposon-based, in-frame, linker insertion mutants of NleD were tested for their ability to cleave JNK and p38 during transient transfection of cultured epithelial cells. Immunoblot analysis of p38 and JNK cleavage showed that 7 mutant derivatives of NleD no longer cleaved p38 but maintained the ability to cleave JNK. Site-directed mutation of specific regions surrounding the insertion sites within NleD revealed that a single amino acid, R203, was essential for cleavage of p38 but not JNK in a direct in vitro cleavage assay, in transiently transfected cells, or in EPEC-infected cells. Mass spectrometry analysis narrowed the cleavage region to within residues 187 and 213 of p38. Mutation of residue R203 within NleD to a glutamate residue abolished the cleavage of p38 and impaired the ability of NleD to inhibit AP-1-dependent gene transcription of a luciferase reporter. Furthermore, the R203 mutation abrogated the ability of NleD to dampen interleukin-6 production in EPEC-infected cells. Overall, this work provides greater insight into substrate recognition and specificity by the type III effector NleD.

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