@article {731901, title = {Pseudomonas syringae manipulates systemic plant defenses against pathogens and herbivores}, journal = {Proceedings of the National Academy of Sciences of the United States of America}, volume = {102}, number = {5}, year = {2005}, note = {

895QFTimes Cited:136Cited References Count:67

Highlighted on\ Faculty of 1000

}, month = {Feb 1}, pages = {1791-1796}, abstract = {

Many pathogens are virulent because they specifically interfere with host defense responses and therefore can proliferate. Here, we report that virulent strains of the bacterial phytopathogen Pseudomonas syringae induce systemic susceptibility to secondary A syringae infection in the host plant Arabidopsis thaliana. This systemic induced susceptibility (SIS) is in direct contrast to the well studied avirulence/R gene-dependent resistance response known as the hypersensitive response that elicits systemic acquired resistance. We show that A syringae-elicited SIS is caused by the production of coronatine (COR), a pathogen -derived functional and structural mimic of the phytohormone jasmonic acid (JA). These data suggest that SIS may be a consequence of the previously described mutually antagonistic interaction between the salicylic acid and JA signaling pathways. Virulent P. syringae also has the potential to induce net systemic susceptibility to herbivory by an insect (Trichoplusia ni, cabbage looper), but this susceptibility is not caused by COR. Rather, consistent with its role as a A mimic, COR induces systemic resistance to T. ni. These data highlight the complexity of defense signaling interactions among plants, pathogens, and herbivores.

}, keywords = {acquired-resistance, arabidopsis, arabidopsis-thaliana, coronatine, cross-talk, gene-expression, induced disease resistance, induced susceptibility, jasmonic acid, methyl jasmonate, npr1-independent expression, phytotoxin coronatine, salicylic-acid, trichoplusia ni}, isbn = {0027-8424}, author = {Cui, J. and Bahrami, A. K. and Pringle, E. G. and Hernandez-Guzman, G. and Bender, C. L. and Pierce, N. E. and Ausubel, F. M.} }