Abstract
Systemic acquired resistance (SAR) is a form of defense that provides resistance against a broad spectrum of pathogens in plants. Previous work indicates a role for plastidial glycerolipid biosynthesis in SAR. Specifically, mutations in FATTY ACID DESATURASE7 (FAD7), which lead to reduced trienoic fatty acid levels and compromised plastidial lipid biosynthesis, have been associated with defective SAR. We show that the defective SAR in Arabidopsis (Arabidopsis thaliana) fad7-1 plants is not associated with a mutation in FAD7 but rather with a second-site mutation in GLABRA1 (GL1), a gene well known for its role in trichome formation. The compromised SAR in gl1 plants is associated with impairment in their cuticles. Furthermore, mutations in two other components of trichome development, GL3 and TRANSPARENT TESTA GLABRA1, also impaired cuticle development and SAR. This suggests an overlap in the biochemical pathways leading to cuticle and trichome development. Interestingly, exogenous application of gibberellic acid (GA) not only enhanced SAR in wild-type plants but also restored SAR in gl1 plants. In contrast to GA, the defense phytohoromes salicylic acid and jasmonic acid were unable to restore SAR in gl1 plants. GA application increased levels of cuticular components but not trichome formation on gl1 plants, thus implicating cuticle, but not trichomes, as an important component of SAR. Our findings question the prudence of using mutant backgrounds for genetic screens and underscore a need to reevaluate phenotypes previously studied in the gl1 background.
Highlights
Plants have evolved a large array of defense mechanisms to resist infection by pathogens.Upon recognition, the host plant initiates one or more signal transduction pathways that activate various plant defenses and thereby prevent pathogen colonization
Our results show that impaired fatty acids (FA)/lipid flux is not associated with compromised Systemic acquired resistance (SAR) in fad[] plants but, rather, an abnormal cuticle, which is the result of a non-allelic mutation in the GL (GLABRA) 1 gene
If any, of the desaturated FA species contributed to SAR, we first evaluated SAR in all fad mutants that are defective in the desaturation of various FA species present on plastidal or extraplastidial membrane lipids
Summary
Plants have evolved a large array of defense mechanisms to resist infection by pathogens.Upon recognition, the host plant initiates one or more signal transduction pathways that activate various plant defenses and thereby prevent pathogen colonization. Genes and the accumulation of salicylic acid (SA) in the inoculated leaf Induction of these responses is accompanied by localized cell death at the site of pathogen entry, which can often restrict the spread of pathogen to cells within and immediately surrounding the lesions. Concurrent with HR development defense reactions are triggered in sites both local and distal from the primary infection This phenomenon, known as systemic acquired resistance (SAR), is accompanied by a local and systemic increase in SA and jasmonic acid (JA) and a concomitant upregulation of a large set of defense genes (Durrant and Dong, 2004; Truman et al, 2007; Vlot et al, 2009)
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