|Block, Anna - HORTICULTURAL DEPT UF|
|Jeffrey, Jones - DEPT PLANT PATH. UF|
|Klee, Harry - HORTICULTURAL DEPT UF|
Submitted to: Molecular Plant Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: November 11, 2004
Publication Date: March 20, 2005
Citation: Block, A., Schmelz, E.A., Jeffrey, J.B., Klee, H.J. 2005. Coronatine and salicylic acid: the battle between arabidopsis and pseudomonas for phytohormone control. Molecular Plant Pathology. 6(1):79-83. Interpretive Summary: Plant pathogens commonly produce toxins and plant hormone mimics to manipulate physiology and thus aid in further pathogen growth. The causal agent of bacterial spec disease in tomato is Pseudomonas syringae pv. tomato (Pst). Pst produces the plant hormone mimic coronatine that is believed to act as a virulence factor in the promotion of bacterial growth. Plant hormones often influence the levels and production of other plant hormones. Thus coronatine may mediate plant responses indirectly by exerting control over other hormone titers. In collaboration with researchers at the University of Florida, scientists at the Center for Medical, Agricultural and Veterinary Entomology in Gainesville, FL, have discovered that coronatine deficient Pst bacteria display lower infection levels in plants with both normal and compromised phytohormone signaling pathways. These results indicate that coronatine acts primarily as a hormone mimic and not through the suppression of other key plant defense hormones, such as salicylic acid. A thorough mechanistic understanding of how infectious bacteria circumvent plant defenses will enable more effective means of pathogen control.
Technical Abstract: The phytotoxin coronatine is a jasmonate mimic produced by Pseudomonas syringae pv. tomato (Pst). Coronatine acts as a virulence factor in Arabidopsis and mutants insensitive to coronatine are resistant to Pst and have higher levels of salicylic acid (SA) (Kloek et al., 2001). In this work we used the SA-deficient lines NahG and sid2-2 to determine if coronatine acts directly as a virulence factor or indirectly by SA suppression. Using coronatine-deficient Pst mutants we demonstrated that the lack of coronatine compromises Pst virulence in both wild type and SA-deficient Arabidopsis. Thus, the action of coronatine is not due to SA suppression. Rather, SA-independent jasmonate responses are the most likely mechanism for its action.