The Pseudomonas type III effector HopQ1 activates cytokinin signaling and interferes with plant innate immunity

The Pseudomonas type III effector HopQ1 activates cytokinin signaling and interferes with plant innate immunity. Hann, D. R., Domínguez‐Ferreras, A., Motyka, V., Dobrev, P. I., Schornack, S., Jehle, A., Felix, G., Chinchilla, D., Rathjen, J. P., & Boller, T. New Phytologist, 201(2):585–598, 2014.
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Summary We characterized the molecular function of the P seudomonas syringae pv. tomato DC 3000 ( Pto ) effector HopQ1. In silico studies suggest that HopQ1 might possess nucleoside hydrolase activity based on the presence of a characteristic aspartate motif. Transgenic A rabidopsis lines expressing HopQ1 or HopQ1 aspartate mutant variants were characterized with respect to flagellin triggered immunity, phenotype and changes in phytohormone content by high‐performance liquid chromatography‐MS ( HPLC ‐ MS ). We found that HopQ1, but not its aspartate mutants, suppressed all tested immunity marker assays. Suppression of immunity was the result of a lack of the flagellin receptor FLS 2, whose gene expression was abolished by HopQ1 in a promoter‐dependent manner. Furthermore, HopQ1 induced cytokinin signaling in A rabidopsis and the elevation in cytokinin signaling appears to be responsible for the attenuation of FLS2 expression. We conclude that HopQ1 can activate cytokinin signaling and that moderate activation of cytokinin signaling leads to suppression of FLS2 accumulation and thus defense signaling.

@article{hann_pseudomonas_2014,
	title = {The \textit{{Pseudomonas}} type {III} effector {HopQ1} activates cytokinin signaling and interferes with plant innate immunity},
	volume = {201},
	doi = {10.1111/nph.12544},
	abstract = {Summary
            
              
                
                  
                    We characterized the molecular function of the
                    
                      P
                      seudomonas syringae
                    
                    pv.
                    tomato
                    DC
                    3000 (
                    
                      Pto
                    
                    ) effector HopQ1.
                  
                
                
                  
                    In silico
                    studies suggest that HopQ1 might possess nucleoside hydrolase activity based on the presence of a characteristic aspartate motif. Transgenic
                    
                      A
                      rabidopsis
                    
                    lines expressing
                    
                      HopQ1
                    
                    or
                    
                      HopQ1
                    
                    aspartate mutant variants were characterized with respect to flagellin triggered immunity, phenotype and changes in phytohormone content by high‐performance liquid chromatography‐MS (
                    HPLC
                    ‐
                    MS
                    ).
                  
                
                
                  
                    We found that HopQ1, but not its aspartate mutants, suppressed all tested immunity marker assays. Suppression of immunity was the result of a lack of the flagellin receptor
                    FLS
                    2, whose gene expression was abolished by HopQ1 in a promoter‐dependent manner. Furthermore, HopQ1 induced cytokinin signaling in
                    
                      A
                      rabidopsis
                    
                    and the elevation in cytokinin signaling appears to be responsible for the attenuation of
                    
                      FLS2
                    
                    expression.
                  
                
                
                  
                    We conclude that HopQ1 can activate cytokinin signaling and that moderate activation of cytokinin signaling leads to suppression of
                    
                      FLS2
                    
                    accumulation and thus defense signaling.},
	number = {2},
	journal = {New Phytologist},
	author = {Hann, Dagmar R. and Domínguez‐Ferreras, Ana and Motyka, Vaclav and Dobrev, Petre I. and Schornack, Sebastian and Jehle, Anna and Felix, Georg and Chinchilla, Delphine and Rathjen, John P. and Boller, Thomas},
	year = {2014},
	pages = {585--598},
}

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Transgenic A rabidopsis lines expressing HopQ1 or HopQ1 aspartate mutant variants were characterized with respect to flagellin triggered immunity, phenotype and changes in phytohormone content by high‐performance liquid chromatography‐MS ( HPLC ‐ MS ). We found that HopQ1, but not its aspartate mutants, suppressed all tested immunity marker assays. Suppression of immunity was the result of a lack of the flagellin receptor FLS 2, whose gene expression was abolished by HopQ1 in a promoter‐dependent manner. Furthermore, HopQ1 induced cytokinin signaling in A rabidopsis and the elevation in cytokinin signaling appears to be responsible for the attenuation of FLS2 expression. We conclude that HopQ1 can activate cytokinin signaling and that moderate activation of cytokinin signaling leads to suppression of FLS2 accumulation and thus defense signaling.","number":"2","journal":"New Phytologist","author":[{"propositions":[],"lastnames":["Hann"],"firstnames":["Dagmar","R."],"suffixes":[]},{"propositions":[],"lastnames":["Domínguez‐Ferreras"],"firstnames":["Ana"],"suffixes":[]},{"propositions":[],"lastnames":["Motyka"],"firstnames":["Vaclav"],"suffixes":[]},{"propositions":[],"lastnames":["Dobrev"],"firstnames":["Petre","I."],"suffixes":[]},{"propositions":[],"lastnames":["Schornack"],"firstnames":["Sebastian"],"suffixes":[]},{"propositions":[],"lastnames":["Jehle"],"firstnames":["Anna"],"suffixes":[]},{"propositions":[],"lastnames":["Felix"],"firstnames":["Georg"],"suffixes":[]},{"propositions":[],"lastnames":["Chinchilla"],"firstnames":["Delphine"],"suffixes":[]},{"propositions":[],"lastnames":["Rathjen"],"firstnames":["John","P."],"suffixes":[]},{"propositions":[],"lastnames":["Boller"],"firstnames":["Thomas"],"suffixes":[]}],"year":"2014","pages":"585–598","bibtex":"@article{hann_pseudomonas_2014,\n\ttitle = {The \\textit{{Pseudomonas}} type {III} effector {HopQ1} activates cytokinin signaling and interferes with plant innate immunity},\n\tvolume = {201},\n\tdoi = {10.1111/nph.12544},\n\tabstract = {Summary\n \n \n \n \n We characterized the molecular function of the\n \n P\n seudomonas syringae\n \n pv.\n tomato\n DC\n 3000 (\n \n Pto\n \n ) effector HopQ1.\n \n \n \n \n In silico\n studies suggest that HopQ1 might possess nucleoside hydrolase activity based on the presence of a characteristic aspartate motif. Transgenic\n \n A\n rabidopsis\n \n lines expressing\n \n HopQ1\n \n or\n \n HopQ1\n \n aspartate mutant variants were characterized with respect to flagellin triggered immunity, phenotype and changes in phytohormone content by high‐performance liquid chromatography‐MS (\n HPLC\n ‐\n MS\n ).\n \n \n \n \n We found that HopQ1, but not its aspartate mutants, suppressed all tested immunity marker assays. Suppression of immunity was the result of a lack of the flagellin receptor\n FLS\n 2, whose gene expression was abolished by HopQ1 in a promoter‐dependent manner. Furthermore, HopQ1 induced cytokinin signaling in\n \n A\n rabidopsis\n \n and the elevation in cytokinin signaling appears to be responsible for the attenuation of\n \n FLS2\n \n expression.\n \n \n \n \n We conclude that HopQ1 can activate cytokinin signaling and that moderate activation of cytokinin signaling leads to suppression of\n \n FLS2\n \n accumulation and thus defense signaling.},\n\tnumber = {2},\n\tjournal = {New Phytologist},\n\tauthor = {Hann, Dagmar R. and Domínguez‐Ferreras, Ana and Motyka, Vaclav and Dobrev, Petre I. and Schornack, Sebastian and Jehle, Anna and Felix, Georg and Chinchilla, Delphine and Rathjen, John P. and Boller, Thomas},\n\tyear = {2014},\n\tpages = {585--598},\n}\n\n\n\n","author_short":["Hann, D. R.","Domínguez‐Ferreras, A.","Motyka, V.","Dobrev, P. I.","Schornack, S.","Jehle, A.","Felix, G.","Chinchilla, D.","Rathjen, J. 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