High-Light-Induced Stress Activates Lipid Deacylation at the Sn-2 Position in the Cyanobacterium Synechocystis Sp. PCC 6803
| Autor: | Nobuyuki Takatani, Kazutaka Ikeda, Sumie Keta, Makiko Aichi, Kouji Kojima, U i Matsumoto, Kenji Nakahigashi, Tatsuo Omata |
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| Rok vydání: | 2021 |
| Předmět: |
Photoinhibition
Light Lipid deacylation Physiology Membrane lipids Mutant Toxicity to FFAs Plant Science Fatty Acids Nonesterified Genes Plant AcademicSubjects/SCI01180 Palmitic acid Membrane Lipids chemistry.chemical_compound Gene Expression Regulation Plant Stress Physiological Regular Paper Cells Cultured biology Adaptation Ocular AcademicSubjects/SCI01210 Acyl-ACP synthetase Synechocystis Cell Biology General Medicine biology.organism_classification Editor's Choice chemistry Biochemistry Mutation lipids (amino acids peptides and proteins) Thiolester Hydrolases Heterologous expression Growth inhibition Intracellular |
| Zdroj: | Plant and Cell Physiology |
| ISSN: | 1471-9053 0032-0781 |
| Popis: | Cyanobacterial mutants defective in acyl-acyl carrier protein synthetase (Aas) produce free fatty acids (FFAs) because the FFAs generated by deacylation of membrane lipids cannot be recycled. An engineered Aas-deficient mutant of Synechocystis sp. PCC 6803 grew normally under low-light (LL) conditions (50 µmol photons m−2 s−1) but was unable to sustain growth under high-light (HL) conditions (400 µmol photons m−2 s−1), revealing a crucial role of Aas in survival under the HL conditions. Several-times larger amounts of FFAs were produced by HL-exposed cultures than LL-grown cultures. Palmitic acid accounted for ∼85% of total FFAs in HL-exposed cultures, while C18 fatty acids (FAs) constituted ∼80% of the FFAs in LL-grown cultures. Since C16 FAs are esterified to the sn-2 position of lipids in the Synechocystis species, it was deduced that HL irradiation activated deacylation of lipids at the sn-2 position. Heterologous expression of FarB, the FFA exporter protein of Neisseria lactamica, prevented intracellular FFA accumulation and rescued the growth defect of the mutant under HL, indicating that intracellular FFA was the cause of growth inhibition. FarB expression also decreased the ‘per-cell’ yield of FFA under HL by 90% and decreased the proportion of palmitic acid to ∼15% of total FFA. These results indicated that the HL-induced lipid deacylation is triggered not by strong light per se but by HL-induced damage to the cells. It was deduced that there is a positive feedback loop between HL-induced damage and lipid deacylation, which is lethal unless FFA accumulation is prevented by Aas. |
| Databáze: | OpenAIRE |
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