scholarly journals Bacterial Type Two Secretion System Secreted Proteins: Double-Edged Swords for Plant Pathogens

2005 ◽  
Vol 18 (9) ◽  
pp. 891-898 ◽  
Author(s):  
Gopaljee Jha ◽  
R. Rajeshwari ◽  
Ramesh V. Sonti
Keyword(s):  
Cell Walls ◽  
Plant Pathogens ◽  
Defense Responses ◽  
Secretion System ◽  
Secreted Proteins ◽  
Plant Cell Walls ◽  
Plant Defense Responses ◽  
Type Three Secretion System ◽  
Type Three Secretion ◽  
Bacterial Type

The type two secretion system (T2S) is important for virulence of a number of gram-negative bacterial plant pathogens. Most of the T2S-secreted proteins that have been characterized to date are involved in degrading different components of plant cell walls. Functional redundancy appears to exist among T2S-secreted proteins because significant effects on virulence are observed only in strains in which multiple secreted proteins are mutated. Several T2S-secreted proteins have been shown to induce plant defense responses, including hypersensitive response-like reactions. Bacterial pathogens can suppress these defense responses, and recent results indicate that suppression is mediated through the type three secretion system.

scholarly journals Ancestral acquisitions, gene flow and multiple evolutionary trajectories of the type three secretion system and effectors in Xanthomonas plant pathogens

2017 ◽  
Vol 26 (21) ◽  
pp. 5939-5952 ◽  
Author(s):  
Déborah Merda ◽  
Martial Briand ◽  
Eran Bosis ◽  
Céline Rousseau ◽  
Perrine Portier ◽  
...  
Keyword(s):  
Gene Flow ◽  
Plant Pathogens ◽  
Secretion System ◽  
Type Three Secretion System ◽  
Evolutionary Trajectories ◽  
Type Three Secretion

scholarly journals Bacterial internalization is required to trigger NIK-dependent NF-κB activation in response to the bacterial type three secretion system

PLoS ONE ◽  
2017 ◽  
Vol 12 (2) ◽  
pp. e0171406 ◽  
Author(s):  
Miles C. Duncan ◽  
Natalia G. Herrera ◽  
Kevin S. Johnson ◽  
Joanne N. Engel ◽  
Victoria Auerbuch
Keyword(s):  
Secretion System ◽  
Type Three Secretion System ◽  
Type Three Secretion ◽  
Bacterial Type

scholarly journals Fusarium graminearum arabinanase (Arb93B) Enhances Wheat Head Blight Susceptibility by Suppressing Plant Immunity

2019 ◽  
Vol 32 (7) ◽  
pp. 888-898 ◽  
Author(s):  
Guixia Hao ◽  
Susan McCormick ◽  
Martha M. Vaughan ◽  
Todd A. Naumann ◽  
Hye-Seon Kim ◽  
...  
Keyword(s):  
Fusarium Graminearum ◽  
Cell Walls ◽  
Fluorescent Protein ◽  
Plant Immunity ◽  
Defense Responses ◽  
Plant Cell Walls ◽  
Plant Defense Responses ◽  
Wild Type ◽  
Head Blight ◽  
Green Fluorescent

Fusarium head blight (FHB) of wheat and barley caused by the fungus Fusarium graminearum reduces crop yield and contaminates grain with mycotoxins. In this study, we investigated two exo-1,5-α-L-arabinanases (Arb93A and Arb93B) secreted by F. graminearum and their effect on wheat head blight development. Arabinan is an important component of plant cell walls but it was not known whether these arabinanases play a role in FHB. Both ARB93A and ARB93B were induced during the early stages of infection. arb93A mutants did not exhibit a detectable change in ability to cause FHB, whereas arb93B mutants caused lower levels of FHB symptoms and deoxynivalenol contamination compared with the wild type. Furthermore, virulence and deoxynivalenol contamination were restored to wild-type levels in ARB93B complemented mutants. Fusion proteins of green fluorescent protein (GFP) with the predicted chloroplast peptide or the mature protein of Arb93B were not observed in the chloroplast. Reactive oxygen species (ROS) production was reduced in the infiltrated zones of Nicotiana benthamiana leaves expressing ARB93B-GFP. Coexpression of ARB93B-GFP and Bax in N. benthamiana leaves significantly suppressed Bax-programmed cell death. Our results indicate that Arb93B enhances plant disease susceptibility by suppressing ROS-associated plant defense responses.

An inhibitory mechanism of action of coiled‐coil peptides against type three secretion system from enteropathogenicEscherichia coli

2019 ◽  
Vol 25 (3) ◽  
Author(s):  
Mariano Larzábal ◽  
Hector A. Baldoni ◽  
Fernando D. Suvire ◽  
Lucrecia M. Curto ◽  
Gabriela E. Gomez ◽  
...  
Keyword(s):  
Mechanism Of Action ◽  
Coiled Coil ◽  
Secretion System ◽  
Inhibitory Mechanism ◽  
Type Three Secretion System ◽  
Type Three Secretion

scholarly journals Plasmid composition in Aeromonas salmonicida subsp. salmonicida 01-B526 unravels unsuspected type three secretion system loss patterns

BMC Genomics ◽  
2017 ◽  
Vol 18 (1) ◽  
Author(s):  
Katherine H. Tanaka ◽  
Antony T. Vincent ◽  
Jean-Guillaume Emond-Rheault ◽  
Marcin Adamczuk ◽  
Michel Frenette ◽  
...  
Keyword(s):  
Secretion System ◽  
Aeromonas Salmonicida ◽  
Type Three Secretion System ◽  
Type Three Secretion

scholarly journals Type Three Secretion System-Dependent Microvascular Thrombosis and Ischemic Enteritis in Human Gut Xenografts Infected with Enteropathogenic Escherichia coli

2017 ◽  
Vol 85 (11) ◽  
Author(s):  
Einat Nissim-Eliraz ◽  
Eilam Nir ◽  
Irit Shoval ◽  
Noga Marsiano ◽  
Israel Nissan ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Blood Vessels ◽  
Secretion System ◽  
Infection Model ◽  
Apical Surface ◽  
Muscularis Mucosa ◽  
Human Gut ◽  
Type Three Secretion System ◽  
Type Three Secretion ◽  
Ischemic Enteritis

ABSTRACT Enteropathogenic Escherichia coli (EPEC) is a leading cause of severe intestinal disease and infant mortality in developing countries. Virulence is mediated by a type three secretion system (T3SS), causing the hallmark attaching and effacing (AE) lesions and actin-rich pedestal formation beneath the infecting bacteria on the apical surface of enterocytes. EPEC is a human-specific pathogen whose pathogenesis cannot be studied in animal models. We therefore established an EPEC infection model in human gut xenografts in SCID mice and used it to study the role of T3SS in the pathogenesis of the disease. Following EPEC O127:H6 strain E2348/69 infection, T3SS-dependent AE lesions and pedestals were demonstrated in all infected xenografts. We report here the development of T3SS-dependent intestinal thrombotic microangiopathy (iTMA) and ischemic enteritis in ∼50% of infected human gut xenografts. Using species-specific CD31 immunostaining, we showed that iTMA was limited to the larger human-mouse chimeric blood vessels, which are located between the muscularis mucosa and circular muscular layer of the human gut. These blood vessels were massively invaded by bacteria, which adhered to and formed pedestals on endothelial cells and aggregated with mouse neutrophils in the lumen. We conclude that endothelial infection, iTMA, and ischemic enteritis might be central mechanisms underlying severe EPEC-mediated disease.

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