scholarly journals Phosphorylation of HopQ1, a Type III Effector from Pseudomonas syringae, Creates a Binding Site for Host 14-3-3 Proteins

2013 ◽  
Vol 161 (4) ◽  
pp. 2049-2061 ◽  
Author(s):  
Fabian Giska ◽  
Małgorzata Lichocka ◽  
Marcin Piechocki ◽  
Michał Dadlez ◽  
Elmon Schmelzer ◽  
...  
2003 ◽  
Vol 49 (6) ◽  
pp. 1537-1546 ◽  
Author(s):  
Michael J. Axtell ◽  
Stephen T. Chisholm ◽  
Douglas Dahlbeck ◽  
Brian J. Staskawicz

2006 ◽  
Vol 62 (1) ◽  
pp. 26-44 ◽  
Author(s):  
Boris A. Vinatzer ◽  
Gail M. Teitzel ◽  
Min-Woo Lee ◽  
Joanna Jelenska ◽  
Sara Hotton ◽  
...  

2007 ◽  
Vol 51 (1) ◽  
pp. 32-46 ◽  
Author(s):  
Chia-Fong Wei ◽  
Brian H. Kvitko ◽  
Rena Shimizu ◽  
Emerson Crabill ◽  
James R. Alfano ◽  
...  

2019 ◽  
Author(s):  
Carolina Mazo-Molina ◽  
Samantha Mainiero ◽  
Sara R. Hind ◽  
Christine M. Kraus ◽  
Mishi Vachev ◽  
...  

AbstractRace 1 strains of Pseudomonas syringae pv. tomato, which causes bacterial speck disease of tomato, are becoming increasingly common and no simply-inherited genetic resistance to such strains is known. We discovered that a locus in Solanum lycopersicoides, termed Pseudomonas tomato race 1 (Ptr1), confers resistance to race 1 Pst strains by recognizing the type III effector AvrRpt2. In Arabidopsis, AvrRpt2 degrades the RIN4 protein thereby activating RPS2-mediated immunity. Ptr1 also recognized homologs of AvrRpt2 from diverse bacteria including one in Ralstonia pseudosolanacearum and this correlated with the ability of AvrRpt2 to degrade RIN4. Using site-directed mutagenesis of AvrRpt2 we found that Ptr1 and RPS2 recognize identical features of AvrRpt2. However, the genome sequence of S. lycopersicoides revealed no RPS2 homolog in the Ptr1 region. Ptr1 could play an important role in controlling bacterial speck disease and its future cloning may shed light on an example of convergent evolution for recognition of a widespread type III effector.


2009 ◽  
Vol 22 (9) ◽  
pp. 1069-1080 ◽  
Author(s):  
Ming Guo ◽  
Fang Tian ◽  
Yashitola Wamboldt ◽  
James R. Alfano

The Pseudomonas syringae type III protein secretion system (T3SS) and the type III effectors it injects into plant cells are required for plant pathogenicity and the ability to elicit a hypersensitive response (HR). The HR is a programmed cell death that is associated with effector-triggered immunity (ETI). A primary function of P. syringae type III effectors appears to be the suppression of ETI and pathogen-associated molecular pattern–triggered immunity (PTI), which is induced by conserved molecules on microorganisms. We reported that seven type III effectors from P. syringae pv. tomato DC3000 were capable of suppressing an HR induced by P. fluorescens(pHIR11) and have now tested 35 DC3000 type III effectors in this assay, finding that the majority of them can suppress the HR induced by HopA1. One newly identified type III effector with particularly strong HR suppression activity was HopS2. We used the pHIR11 derivative pLN1965, which lacks hopA1, in related assays and found that a subset of the type III effectors that suppressed HopA1-induced ETI also suppressed an ETI response induced by AvrRpm1 in Arabidopsis thaliana. A. thaliana plants expressing either HopAO1 or HopF2, two type III effectors that suppressed the HopA1-induced HR, were reduced in the flagellin-induced PTI response as well as PTI induced by other PAMPs and allowed enhanced in planta growth of P. syringae. Collectively, our results suggest that the majority of DC3000 type III effectors can suppress plant immunity. Additionally, the construct pLN1965 will likely be a useful tool in determining whether other type III effectors or effectors from other types of pathogens can suppress either ETI, PTI, or both.


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