Cellular membrane accommodation of copper-induced oxidative conditions in the coral Seriatopora caliendrum

• Coral cells alter membrane lipid to accommodate copper-induce oxidative conditions
• Coral membrane repair occur due to lipid alterations
• Zooxanthellae release results from membrane repair by symbiosome fusion
• Copper-induced lipid alterations perturb membrane-related functions in coral cells
• Copper chronic effect on coral fitness are related to long-term membrane perturbation

Oxidative stress has been associated with copper-induced toxicity in scleractinian corals. To gain insight into the accommodation of the cellular membrane to oxidative conditions, a pocilloporid coral, Seriatopora caliendrum, was exposed to copper at distinct, environmentally relevant dose for various lengths of time. Glycerophosphocholine profiling of the response of the coral to copper exposure was characterized using a validated method. The results indicate that coral lipid metabolism is programmed to induce membrane alterations in response to the cellular deterioration that occurs during the copper exposure period. Decreasing lyso-phosphatidylcholines and exchanging polyunsaturated phosphatidylcholines for polyunsaturated plasmanylcholines were the initial actions taken to prevent membrane permeabilization. To relax/resist the resulting membrane strain caused by cell/organelle swelling, the coral cells inversely exchanged polyunsaturated plasmanylcholines for polyunsaturated phosphatidylcholines and further increased the levels of monounsaturated glycerophosphocholines. At the same time, the levels of saturated phosphatidylcholines were also increased to increase membrane rigidity and protect against oxidative attack. Interestingly, such alterations in lipid metabolism were also required for membrane fusion to repair the deteriorated membranes by repopulating them with proximal lipid reservoirs, similar to symbiosome membranes. Additionally, increasing saturated and monounsaturated plasmanylcholines and inhibiting the suppression of saturated lyso-phosphatidylcholines were shown to facilitate membrane fusion. Based on the biochemical and biophysical properties of these lipids, the chronic effects of copper, such as coral resistance and growth, can be logically interpreted to result from long-term perturbations in cellular membrane-related functions. In conclusion, the cells of S. caliendrum alter their lipid metabolism and sacrifice fitness to allow the membrane to accommodate copper-induced oxidative situations.