Misexpression of FATTY ACID ELONGATION1 in the Arabidopsis epidermis induces cell death and suggests a critical role for phospholipase A2 in this process

Max-Planck-Institut für Züchtungsforschung, 50829 Köln, Germany.
The Plant Cell (Impact Factor: 9.34). 05/2009; 21(4):1252-72. DOI: 10.1105/tpc.109.065565
Source: PubMed


Very-long-chain fatty acids (VLCFAs) are important functional components of various lipid classes, including cuticular lipids in the higher plant epidermis and lipid-derived second messengers. Here, we report the characterization of transgenic Arabidopsis thaliana plants that epidermally express FATTY ACID ELONGATION1 (FAE1), the seed-specific beta-ketoacyl-CoA synthase (KCS) catalyzing the first rate-limiting step in VLCFA biosynthesis. Misexpression of FAE1 changes the VLCFAs in different classes of lipids but surprisingly does not complement the KCS fiddlehead mutant. FAE1 misexpression plants are similar to the wild type but display an essentially glabrous phenotype, owing to the selective death of trichome cells. This cell death is accompanied by membrane damage, generation of reactive oxygen species, and callose deposition. We found that nuclei of arrested trichome cells in FAE1 misexpression plants cell-autonomously accumulate high levels of DNA damage, including double-strand breaks characteristic of lipoapoptosis. A chemical genetic screen revealed that inhibitors of KCS and phospholipase A2 (PLA2), but not inhibitors of de novo ceramide biosynthesis, rescue trichome cells from death. These results support the functional role of acyl chain length of fatty acids and PLA2 as determinants for programmed cell death, likely involving the exchange of VLCFAs between phospholipids and the acyl-CoA pool.

Download full-text


Available from: Jose Juan Reina-Pinto, Jan 30, 2014
  • Source
    • "Together, these observations support the notion that GA-mediated restoration of cuticle might be responsible for the restored SAR in gl1 plants. More importantly, these and our earlier results (Xia et al., 2009) reconfirm the fact that cuticle-deficient mutants are impaired in their ability to perceive mobile signal. "
    [Show abstract] [Hide abstract]
    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.
    Full-text · Article · Oct 2010 · Plant physiology
  • [Show abstract] [Hide abstract]
    ABSTRACT: This paper addresses the minimum initial marking (MIM) in timed marked graphs. In this problem both the net and the cycle time are fixed, so the problem consists in finding out a minimum initial marking M<sub>0</sub> such that the cycle time of the TMG will be less or equal to the required one. The main result of this work is the heuristic algorithm MIM Solver to solve the MIM problem. It computes a subset of p-semiflows and adds tokens to places in two steps. First it adds the minimum number of tokens needed to reduce the difference between the required cycle time π<sup>d</sup> and the cycle time π<sub>i</sub> of each p-semiflow belonging to the computed subset. The difference π <sup>d</sup>-π<sub>i</sub>>0 must be minimum. In this step a heuristic based on the places belonging to the maximum number of p-semiflows is used. Afterwards, the algorithm adds the largest number of tokens in p-semiflows to fulfil cycle time constraints. In this step a heuristic based on the places belonging to the shortest number of p-semiflows is used
    No preview · Conference Paper · Feb 2000
  • [Show abstract] [Hide abstract]
    ABSTRACT: This paper deals with the initialization of the discrete wavelet transform. A simple and novel initialization scheme is proposed to demonstrate the relationship between the initialization error and the signal sampling rate as well as the selection of the initialization scaling space. It is also pointed out that the initialization error has a link with the Nyquist sampling theorem
    No preview · Conference Paper · Feb 2000
Show more