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Salicylic Acid Is Part of theMi-1-Mediated Defense Response to Root-Knot Nematode in Tomato
Author(s) -
Craig Branch,
ChinFeng Hwang,
Duroy A. Navarre,
Valerie M. Williamson
Publication year - 2004
Publication title -
molecular plant-microbe interactions
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.565
H-Index - 153
eISSN - 1943-7706
pISSN - 0894-0282
DOI - 10.1094/mpmi.2004.17.4.351
Subject(s) - salicylic acid , biology , root knot nematode , lycopersicon , nematode , systemic acquired resistance , hypersensitive response , nicotiana benthamiana , microbiology and biotechnology , botany , plant disease resistance , gene , biochemistry , ecology , arabidopsis , mutant
The Mi-1 gene of tomato confers resistance against three species of root-knot nematode in tomato (Lycopersicon esculentum). Transformation of tomato carrying Mi-1 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. Exogenous SA was toxic to roots expressing NahG but not to control roots. This toxicity is most likely due to the production of catechol from SA, and we report here that 100 microM catechol is toxic to tomato roots. Benzothiadiazole, a SA analog, completely 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 prevented by coexpression of NahG. These results indicate that SA is an important component of the signaling that leads to nematode resistance and the associated hypersensitive response.

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