The PPR protein RARE1-mediated editing of chloroplast accD transcripts is required for fatty acid biosynthesis and heat tolerance in Arabidopsis
作者全名："Huang, Chao; Liu, Dan; Li, Zi-Ang; Molloy, David P.; Luo, Zhou-Fei; Su, Yi; Li, Hai-Ou; Liu, Qing; Wang, Ruo-Zhong; Xiao, Lang-Tao"
作者地址："[Huang, Chao; Liu, Dan; Li, Zi-Ang; Luo, Zhou-Fei; Su, Yi; Li, Hai-Ou; Liu, Qing; Wang, Ruo-Zhong; Xiao, Lang-Tao] Hunan Agr Univ, Coll Biosci & Biotechnol, Changsha 410128, Peoples R China; [Molloy, David P.] Chongqing Med Univ, Sch Basic Med Sci, Dept Biochem & Mol Biol, Chongqing 400016, Peoples R China"
通信作者："Xiao, LT (通讯作者)，Hunan Agr Univ, Coll Biosci & Biotechnol, Changsha 410128, Peoples R China."
关键词：chloroplast RNA editing; RARE1; accD; fatty acid; heat stress
摘要："It has been reported that Arabidopsis chloroplast accD transcripts undergo RNA editing and that loss of accD-C794 RNA editing does not affect plant growth under normal conditions. To date, the exact biological role of accD-C794 editing has remained elusive. Here, we reveal an unexpected role for accD-C794 editing in response to heat stress. Loss of accD-C794 editing results in a yellow and dwarf phenotype with decreased chloroplast gene expression under heat stress, and artificial improvement of C794-edited accD gene expression enhances heat tolerance in Arabidopsis. These data suggest that accD-C794 editing confers heat tolerance in planta. We also found that treatment with the product of acetyl coenzyme A carboxylase (ACCase) could allay mutant phenotypic characteristics and showed that a mutation in the CAC3 gene for the a-subunit of ACCase was associated with dwarfism under heat stress. These obser-vations indicate that defective accD-C794 editing may be intrinsic to reduced ACCase activity, thereby contributing to heat sensitivity. ACCase catalyzes the committed step of de novo fatty acid (FA) biosyn-thesis. FA content analysis revealed that unsaturated oleic (C18:1) and linoleic acids (C18:2) were low in the accD-C794 editing-defective mutant but high in the C794-edited accD-overexpressing plants compared with the wild type. Supplying exogenous C18:1 and C18:2 could rescue the mutant phenotype, suggesting that these FAs play an essential role in tolerance to heat stress. Transmission electron microscopy obser-vations showed that heat stress seriously affected the membrane architecture in accD editing-defective mutants but not in accD-overexpressing plants. These results provide the first evidence that accD-C794 ed-iting regulates FA biosynthesis for maintenance of membrane structural homeostasis under heat stress."
基金机构："National Natural Science Foundation of China [91317312, 31900387]; Natural Science Foundation of Hunan Province [2020JJ4037, 2021JJ40243]"
基金资助正文：This work was supported by the National Natural Science Foundation of China (91317312 and 31900387) and the Natural Science Foundation of Hunan Province (2020JJ4037 and 2021JJ40243) .