ARS | Publication request: METABOLITE SIGNALING; ROLE OF FATTY ACIDS IN PLANT DEFENSE

Submitted to: Molecular Plant Microbe Interactions
Publication Type: Book / Chapter
Publication Acceptance Date: October 1, 2005
Publication Date: October 1, 2008
Citation: Kachroo, A., Venugopal, S.C., Navarre, D.A., Lapchyk, L., Kachroo, P*. (2006) Metabolite signaling; role of fatty acids in plant defense. In 'Biology of Molecular Plant-Microbe Interactions', Eds, F. Sanchez, C. Quinto, I. M. Lopez-Lara, O. Geiger. 5: 195-201.

Technical Abstract: Stearoyl-ACP-desaturase-mediated conversion of stearic acid (18:0) to oleic acid (18:1) is the key step regulating levels of unsaturated fatty acids (FAs) in the cell. A mutation in the ssi2 encoded S-ACP-DES results in constitutive activation of salicylic acid (SA) pathway and repression of certain jasmonic acid (JA)-mediated responses. Our studies with ssi2/ fab2 and its suppressors indicate that reduced 18:1 levels in these plants are responsible for altered defense signaling. Furthermore, replenishing 18:1 levels results in restoration of wild-type (wt)-like signaling in the mutant. This suggests that 18:1 or an 18:1 derived molecule(s) participates in the SA- and JA-mediated defense signaling pathways of Arabidopsis. We have identified four genes, which participate in the prokaryotic FA pathway and loss-of-function of which restores various SA and JA regulated phenotypes in ssi2 plants. Mutations in the genes encoding for glycerol-3-phosphate (G3P) acyltransferase (ACT1) and G3P dehydrogenase (GLY1) restores wt-like phenotypes in the ssi2 plants. A loss-of-function mutation in oleate- and linolate-desaturase also confers partial restoration of morphological phenotype but does not restore altered defense signaling. Interestingly, the 18:1 content in wt plants can be lowered by exogenous glycerol application, converting these plants to ssi2-mimics. Analyses of mutants impaired in SA signaling or FA pathway has revealed that glycerol induces SA-signaling via the SID2-dependent pathway. The act1 mutant also does not show any reduction in 18:1 levels due to its inability to acylate G3P with 18:1. Consequently, plants overexpressing the ACT1 gene are hypersensitive to exogenous glycerol application. Thus, we demonstrate that 18:1 levels in plastids are regulated via acylation with G3P and a balance between G3P and 18:1 is critical for the regulation of SA- and JA-mediated signaling pathways.