한빛사 논문
Bingqi Lia,b,d, Jun Fanga,b,d, Rahul Mohan Singha, Hailing Zia, Shanshan Lva, Renyi Liuc, Vivek Dograa,e,f, and Chanhong Kima,b,f
a Shanghai Center for Plant Stress Biology and CAS Center for Excellence in Molecular Plant
Sciences, Chinese Academy of Sciences, Shanghai 200032, China
b University of the Chinese Academy of Sciences, Beijing 100049, China
c Center for Agroforestry Mega Data Science and FAFU-UCR Joint Center for Horticultural
Biology and Metabolomics, Haixia Institute of Science and Technology, Fujian Agricultural
and Forestry University, Fuzhou 350002, China
d These authors contributed equally to this work
e Present address: Biotechnology Division, CSIR-Institute of Himalayan Bioresource
Technology, Palampur 176061, India
f Address correspondence
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 thaliana deficient in plastid division, thereby developing gigantic chloroplasts (GC). 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.
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