4.7 Article

Thermal protection function of camphor on Cinnamomum camphora cell membrane by acting as a signaling molecule

Journal

PLANT PHYSIOLOGY AND BIOCHEMISTRY
Volume 198, Issue -, Pages -

Publisher

ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.plaphy.2023.107672

Keywords

Camphor; Membrane lipid; Signaling molecule; Thermotolerance; Ultrastructure

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Isoprenoids, such as camphor released by Cinnamomum camphora, protect plant membranes against high temperature damage by maintaining membrane lipid stabilization. This study investigated the effects of camphor fumigation on membrane permeability, cell ultrastructure, membrane lipid variations, and gene expression in C. camphora under high temperature conditions. The results suggest that camphor acts as a signaling molecule and regulates the expression of genes related to lipid metabolism, thereby protecting the membrane system.
Isoprenoids serve important functions in protecting plant membranes against high temperature. Cinnamomum camphora is an excellent economic tree species, and releases plenty of monoterpenes. To uncover the protective mechanism of monoterpenes on the membrane system for promoting their development and utilization as antihigh temperature agents, the membrane permeability, cell ultrastructure, membrane lipid variations and related gene expression were investigated in C. camphora fumigated with camphor, one of the main monoterpenes in the plant, after fosmidomycin (Fos) blocking the monoterpene biosynthesis under high temperature (Fos+38 degrees C + C). High temperature at 38 degrees C caused the rupture of plasma as well as chloroplast and mitochondrion membranes, deformation of chloroplasts and mitochondria, and electrolyte leakage in C. camphora. High temperature with Fos treatment (Fos+38 degrees C) aggravated the damage, while camphor fumigation (Fos+38 degrees C + C) showed alleviating effects. High temperature at 38 degrees C disturbed the membrane lipid equilibrium by reducing the levels of 14 phosphatidylcholine, 8 phosphatidylglycerol and 6 phosphatidylethanolamine molecules, and increasing the levels of 8 phosphatidic acid, 4 diacylglycerol, 5 phosphatidylinositol, 16 sphingomyelin and 5 ceramide phosphoethanolamine molecules. Fos+38 degrees C treatment primarily exhibited intensifying effects on the disturbance, while these membrane lipid levels in Fos+38 degrees C + C5 (5 mu M camphor) treatment exhibited variation tendencies to the control at 28 degrees C. This should result from the expression alterations of the genes related with phospholipid biosynthesis, fatty acid metabolism, and sphingolipid metabolism. It can be speculated that camphor can maintain membrane lipid stabilization in C. camphora under high temperature by acting as a signaling molecule.

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