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

ABSTRACT

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 anti-high 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 °C + C). High temperature at 38 °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 °C) aggravated the damage, while camphor fumigation (Fos+38 °C + C) showed alleviating effects. High temperature at 38 °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 °C treatment primarily exhibited intensifying effects on the disturbance, while these membrane lipid levels in Fos+38 °C + C5 (5 µM camphor) treatment exhibited variation tendencies to the control at 28 °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.