Inhibition of photosynthetic electron transport by palmitoleic acid is partially correlated to loss of thylakoid membrane proteins

Palmitoleic acid (16:1Δ9), a monounsaturated fatty acid, is found to inhibit electron transport. Inhibition occurs rapidly (within 30 s). The oxidizing side of photosystem (PS) II is ~ 90% inactivated, whereas no inhibition occurs on the reducing side of the PSII complex. PSI activity is ∼ 65% inhibited. Inhibition of electron transport is not correlated to lipid peroxidation. 16:1 causes the loss of proteins from the thylakoid membrane which is exacerbated by the light. The loss of five proteins, viz. plastocyanin (PC), manganese stabilizing protein (MSP), cytochrome f (Cyt f), D1 and D2 is examined. The proteins are found to be lost in the following order: PC (< 1 min), MSP (~5 min), Cyt f (~10 min), D1 (~60 min) and D2 (~60 min). The timing of the loss of a PSI associated protein, PC, overlaps with that of the inhibition of PSI. Also, preventing the loss of PC with spermine (spm) treatment can partially protect PSI from 16:1 inhibition. Thus, the results suggest that the loss of PC is the cause of PSI inhibition. On the other hand, the loss of MSP from the oxygen-evolving complex is not likely to be the cause of the 16:1 inhibition on the oxidizing side of PSII, as the MSP loss occurs later than the inhibition. Also, increased retention of MSP with spm treatment does not relieve the 16:1 inhibition of PSII. Instead, inhibition of PSII by 16:1 is prevented by Mn2+ treatment, suggesting that loss of Mn2+ ions is the cause of PSII inhibition.