1. FATTY ACID DESATURASE5 Is Required to Induce Autoimmune Responses in Gigantic Chloroplast Mutants of Arabidopsis
- Author
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Bingqi Li, Jun Fang, Chanhong Kim, Shanshan Lv, Hailing Zi, Rahul Mohan Singh, Renyi Liu, and Vivek Dogra
- Subjects
Fatty Acid Desaturases ,0106 biological sciences ,0301 basic medicine ,Chloroplasts ,Mutant ,Arabidopsis ,Palmitic Acid ,Cyclopentanes ,Plant Science ,01 natural sciences ,In Brief ,Transcriptome ,03 medical and health sciences ,chemistry.chemical_compound ,Gene Expression Regulation, Plant ,Genes, Chloroplast ,Palmitoleic acid ,Plant Immunity ,Oxylipins ,Plastids ,chemistry.chemical_classification ,Regulation of gene expression ,Reactive oxygen species ,Cell Death ,biology ,Arabidopsis Proteins ,food and beverages ,Fatty acid ,Cell Biology ,Plants, Genetically Modified ,biology.organism_classification ,Cell biology ,Plant Leaves ,030104 developmental biology ,chemistry ,Mutation ,Retrograde signaling ,Salicylic Acid ,010606 plant biology & botany - Abstract
Chloroplasts mediate genetically controlled cell death via chloroplast-to-nucleus retrograde signaling. To decipher the mechanism, we examined chloroplast-linked lesion-mimic mutants of Arabidopsis (Arabidopsis thaliana) deficient in plastid division, thereby developing gigantic chloroplasts (GCs). These GC mutants, including crumpled leaf (crl), constitutively express immune-related genes and show light-dependent localized cell death (LCD), mirroring typical autoimmune responses. Our reverse genetic approach excludes any potential role of immune/stress hormones in triggering LCD. Instead, transcriptome and in silico analyses suggest that reactive electrophile species (RES) generated via oxidation of polyunsaturated fatty acids (PUFAs) or lipid peroxidation-driven signaling may induce LCD. Consistent with these results, the one of the suppressors of crl, dubbed spcrl4, contains a causative mutation in the nuclear gene encoding chloroplast-localized FATTY ACID DESATURASE5 (FAD5) that catalyzes the conversion of palmitic acid (16:0) to palmitoleic acid (16:1). The loss of FAD5 in the crl mutant might attenuate the levels of RES and/or lipid peroxidation due to the reduced levels of palmitic acid-driven PUFAs, which are prime targets of reactive oxygen species. The fact that fad5 also compromises the expression of immune-related genes and the development of LCD in other GC mutants substantiates the presence of an intrinsic retrograde signaling pathway, priming the autoimmune responses in a FAD5-dependent manner.
- Published
- 2020