In this study, the tolerance to salt stress of the photosynthetic machinery was examined in relation to the effects of the genetic enhancement of the unsaturation of fatty acids in membrane lipids in wild-type and desA ϩ cells of Synechococcus sp. PCC 7942. Wild-type cells synthesized saturated and mono-unsaturated fatty acids, whereas desA ϩ cells, which had been transformed with the desA gene for the ⌬12 acyl-lipid desaturase of Synechocystis sp. PCC 6803, also synthesized diunsaturated fatty acids. Incubation of wild-type and desA ϩ cells with 0.5 m NaCl resulted in the rapid loss of the activities of photosystem I, photosystem II, and the Na ϩ /H ϩ antiport system both in light and in darkness. However, desA ϩ cells were more tolerant to salt stress and osmotic stress than the wild-type cells. The extent of the recovery of the various photosynthetic activities from the effects of 0.5 m NaCl was much greater in desA ϩ cells than in wild-type cells. The photosystem II activity of thylakoid membranes from desA ϩ cells was more resistant to 0.5 m NaCl than that of membranes from wild-type cells. These results demonstrated that the genetically engineered increase in unsaturation of fatty acids in membrane lipids significantly enhanced the tolerance of the photosynthetic machinery to salt stress. The enhanced tolerance was due both to the increased resistance of the photosynthetic machinery to the salt-induced damage and to the increased ability of desA ϩ cells to repair the photosynthetic and Na ϩ /H ϩ antiport systems.Salt stress is one of the main environmental factors that limit the growth and productivity of plants and micro-organisms. We have been investigating the mechanisms of the hyperosmotic stress-induced and the salt stress-induced inactivation of the photosynthetic machinery, focussing on the oxygen-evolving machinery of the photosystem II complex, which is the system that is most susceptible to such environmental stress in Synechococcus sp. PCC 7942 (hereafter Synechococcus; Allakhverdiev et al., 2000aAllakhverdiev et al., , 2000b. Hyperosmotic stress due to 1.0 m sorbitol induces the efflux of water through water channels and reduces the volume of cells by more than 50%. This loss of water from the cytosol might be expected to increase the intracellular concentration of salts, and it leads to the rapid but reversible inactivation of the oxygenevolving machinery (Allakhverdiev et al., 2000b).Salt stress due to 0.5 m NaCl has both osmotic and ionic effects (Allakhverdiev et al., 2000a). The osmotic effect due to 0.5 m NaCl is not as strong as the effect of 1.0 m sorbitol and inactivates reversibly the oxygen-evolving machinery. The ionic effect of 0.5 m NaCl is caused by the influx of Na ϩ ions through K ϩ (Na ϩ ) channels and the resultant increase in the intracellular concentration of Na ϩ ions and counterpart anions that are mostly Cl Ϫ ions (Allakhverdiev et al., 2000a). These changes result in the irreversible inactivation of the oxygen-evolving machinery. As a consequence salt stress appears t...