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  4. A Pseudomonas syringae pv. tomato DC3000 mutant lacking the type III effector HopQ1-1 is able to cause disease in the model plant Nicotiana benthamiana
 
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A Pseudomonas syringae pv. tomato DC3000 mutant lacking the type III effector HopQ1-1 is able to cause disease in the model plant Nicotiana benthamiana

Journal
Plant Journal
Journal Volume
51
Journal Volume
51
Journal Issue
1
Journal Issue
1
Pages
32-46
Start Page
32
End Page
46
ISSN
1365313X
Date Issued
2007-07
Author(s)
Wei, Chia-Fong
Kvitko, Brian H.
Shimizu, Rena
Crabill, Emerson
Alfano, James R.
NAI-CHUN LIN  
Martin, Gregory B.
Huang, Hsiou-Chen
Collmer, Alan
DOI
10.1111/j.1365-313X.2007.03126.x
URI
https://scholars.lib.ntu.edu.tw/handle/123456789/446208
https://www.scopus.com/pages/publications/34250807791?origin=resultslist
URL
https://www2.scopus.com/inward/record.uri?eid=2-s2.0-34250807791&doi=10.1111%2fj.1365-313X.2007.03126.x&partnerID=40&md5=2953c9ed6cc8b3228aad684aff9672e5
Abstract
The model pathogen Pseudomonas syringae pv. tomato DC3000 causes bacterial speck in tomato and Arabidopsis, but Nicotiana benthamiana, an important model plant, is considered to be a non-host. Strain DC3000 injects approximately 28 effector proteins into plant cells via the type III secretion system (T3SS). These proteins were individually delivered into N. benthamiana leaf cells via T3SS-proficient Pseudomonas fluorescens, and eight, including HopQ1-1, showed some capacity to cause cell death in this test. Four gene clusters encoding 13 effectors were deleted from DC3000: cluster II (hopH1, hopC1), IV (hopD1, hopQ1-1, hopR1), IX (hopAA1-2, hopV1, hopAO1, hopG1), and native plasmid pDC3000A (hopAM1-2, hopX1, hopO1-1, hopT1-1). DC3000 mutants deleted for cluster IV or just hopQ1-1 acquired the ability to grow to high levels and produce bacterial speck lesions in N. benthamiana. HopQ1-1 showed other hallmarks of an avirulence determinant in N. benthamiana: expression in the tobacco wildfire pathogen P. syringae pv. tabaci 11528 rendered this strain avirulent in N. benthamiana, and elicitation of the hypersensitive response in N. benthamiana by HopQ1-1 was dependent on SGT1. DC3000 polymutants involving other effector gene clusters in a hopQ1-1-deficient background revealed that clusters II and IX contributed to the severity of lesion symptoms in N. benthamiana, as well as in Arabidopsis and tomato. The results support the hypothesis that the host ranges of P. syringae pathovars are limited by the complex interactions of effector repertoires with plant anti-effector surveillance systems, and they demonstrate that N. benthamiana can be a useful model host for DC3000.
Subjects
Avr proteins
Host specificity
Hrp system
Hypersensitive response and pathogenicity
Plant defense
SDGs

[SDGs]SDG3

Type
journal article

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