Department of Plant Pathology, University of Kentucky, Lexington, KY 40546, USA.
Inoculation of Turnip Crinkle Virus (TCV) on the resistant Arabidopsis ecotype Di-17 elicits hypersensitive response (HR), accompanied by increased expression of defense genes. HR to TCV is conferred by HRT, which encodes a CC-NBS-LRR class of resistance (R) protein. In contrast to HR, resistance requires HRT and a recessive locus designated rrt. Unlike most CC-NBS-LRR R proteins, HRT-mediated resistance is dependent on EDS1 and independent of NDR11. Resistance is also independent of RAR1 and SGT1 but is compromised in salicylic acid (SA) deficient eds5, pad4 or sid2 mutants. HRT-mediated HR and resistance are also dependent on light2. A dark treatment, immediately following TCV inoculation, suppresses HR, resistance and activation of a majority of the TCV-induced genes. Interestingly, high endogenous SA due to the ssi2 or cpr5 mutation, confers resistance to TCV, in an HRT-dependent but rrt-independent manner3. The SSI2 gene encodes stearoyl-ACP-desaturase (S-ACP-DES), which catalyzes synthesis of monounsaturated fatty acid, oleic acid (18:1). A mutation in ssi2 results in the alteration of SA- and jasmonic acid-mediated defense responses4–7. The 18:1-mediated pathway regulates defense by upregulating expression of HRT as well as several other R genes. Normalizing 18:1 levels by second-site mutations restores R gene expression. Intriguingly, TCV inoculation does not activate the 18:1-regulated pathway in resistant plants, instead it results in the induction of several genes that encode 18:1-synthesizing isozymes. Consequently 18:1 levels in the plant remain constant during a resistance response to TCV. These data suggest that the 18:1-regulated pathway may be specifically targeted during pathogen infection and that alterations of 18:1 levels may serve as a novel strategy for promoting disease resistance.
