|Branch, Craig - UC DAVIS|
|Hwang, Chin Feng - UC DAVIS|
|Williamson, Valerie - UC DAVIS|
Submitted to: Molecular Plant Microbe Interactions
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: November 17, 2003
Publication Date: April 20, 2004
Citation: Branch, C., Hwang, C., Navarre, D.A., Williamson, V.M. 2004. Salicylic acid is part of the Mi-1-mediated defense response to root-knot nematode in tomato. Molecular Plant Microbe Interactions. 17(4):351-6. Interpretive Summary: Root-knot nematodes are serious pests of both tomato and potato, two closely related plants. The first nematode resistant R-gene Mi-1 was discovered in tomato and closely related genes have since been found in potato. Mechanisms of resistance to root-knot nematodes are likely to be similar between potato and tomato. This paper shows that salicylic acid, an important defense signal molecule in resistance responses to microbial pathogens is also involved in helping plants resist nematode infection. This gives us an important insight about what type of mechanisms are used by plants to resist nematodes and is the first time SA-mediated signaling has shown to be involved in nematode disease resistance.
Technical Abstract: The Mi-1 gene of tomato confers resistance against three species of root-knot nematode in tomato (Lycopersicon esculentum). Transformation of tomato carrying the Mi-1 gene with a construct expressing NahG, which encodes salicylate hydroxylase, a bacterial enzyme that degrades salicylic acid (SA) to catechol, results in partial loss of resistance to root-knot nematodes. NahG expression also renders tomato roots sensitive to exogenous SA. This sensitivity is most likely due to the production of catechol from SA as we have found that catechol is toxic to tomato roots. Benzothiadiazole (BTH), a SA analog, restores nematode resistance in Mi-1 roots transformed with NahG, but does not confer resistance to susceptible tomato roots. The localized cell death produced by transient expression in Nicotiana benthamiana of Mi-DS4, a constitutively lethal chimera of Mi-1 with one of its homologs, was inhibited by co-expression with NahG. These results indicate that SA is an important component of the signaling that leads to nematode resistance and the associated hypersensitive response.