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Published on: May 24, 2018
Two Pantoea agglomerans type III effectors can transform nonpathogenic and phytopathogenic bacteria into
Gal Nissan1,2, Laura Chalupowicz2, Guido Sessa1
1School of Plant Sciences and Security, Faculty of Life Sciences, Tel-Aviv University, Tel Aviv, Israel.
Pantoea agglomerans evolved into pathogens by acquiring a type III secretion system (T3SS) and effectors (T3Es). Specific T3Es, HsvG and PthG, induced galls on gypsophila, while HsvB and PseB induced galls on beet.
Area of Science:
- Plant pathology
- Bacterial genetics
- Molecular biology
Background:
- Pantoea agglomerans (Pa) has evolved into host-specific pathogens causing galls on gypsophila and beet.
- This pathogenicity is linked to acquiring a plasmid encoding a type III secretion system (T3SS) and effectors (T3Es).
- Specific pathovars, Pantoea agglomerans pv. gypsophilae (Pag) and Pantoea agglomerans pv. betae (Pab), exhibit distinct host specificities and virulence factors.
Purpose of the Study:
- To determine the minimal combinations of T3Es sufficient for inducing gall symptoms.
- To investigate the role of specific T3Es in host-specific gall formation.
- To understand the genetic basis of pathogenicity in Pantoea agglomerans.
Main Methods:
- Nonpathogenic and phytopathogenic bacterial strains were transformed with a T3SS-encoding plasmid (pHIR11).
- Transformed strains were further engineered to express individual or paired T3Es: hsvG, hsvB, pthG, and pseB.
- These engineered strains were used to inoculate gypsophila and beet plants to assess gall formation.
Main Results:
- Bacterial strains expressing hsvG and pthG induced galls on gypsophila, regardless of their nonpathogenic or phytopathogenic origin.
- Strains expressing hsvB and pseB induced galls on beet, with the exception of Escherichia coli.
- This indicates that specific T3Es are sufficient to confer host-specific gall-inducing ability.
Conclusions:
- The T3Es HsvG and PthG are sufficient to elicit gall symptoms on gypsophila.
- The T3Es HsvB and PseB are sufficient to elicit gall symptoms on beet.
- These findings highlight the critical role of T3Es in bacterial pathogenicity and host specificity.
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