Plant Physiol, April 2001, Vol. 125, pp. 1842-1853
Unsaturated Fatty Acids in Membrane Lipids Protect the
Photosynthetic Machinery against Salt-Induced Damage in
Synechococcus1
Suleyman I.
Allakhverdiev,
Mikio
Kinoshita,
Masami
Inaba,
Iwane
Suzuki, and
Norio
Murata*
Department of Regulation Biology, National Institute for Basic
Biology, Okazaki 444-8585, Japan (S.I.A., M.K., M.I., I.S., N.M.);
Institute of Basic Biological Problems, Russian Academy of Sciences,
Pushchino, Moscow Region 142292, Russia (S.I.A.); and Department of
Bioresource Science, Obihiro University of Agriculture and Veterinary
Medicine, Inada-cho, Obihiro, Hokkaido 080-8555, Japan (M.K.)
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+ cells of
Synechococcus sp. PCC 7942. Wild-type cells synthesized saturated and mono-unsaturated fatty acids, whereas
desA+ cells, which had been transformed with
the desA gene for the 
12 acyl-lipid desaturase of
Synechocystis sp. PCC 6803, also synthesized
di-unsaturated fatty acids. Incubation of wild-type and
desA+ cells with 0.5 M NaCl
resulted in the rapid loss of the activities of photosystem I,
photosystem II, and the Na+/H+ antiport system
both in light and in darkness. However,
desA+ 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+ cells than in wild-type cells. The
photosystem II activity of thylakoid membranes from
desA+ 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+ cells to repair
the photosynthetic and Na+/H+ antiport systems.
1
This work was supported by a Grant-in-Aid for
Specially Promoted Research from the Ministry of Education, Science and
Culture, Japan (grant no. 08102011 to N.M.), and in part by the
National Institute for Basic Biology Cooperative Research Program on
the Stress Tolerance of Plants. S.I.A. was the recipient of an
Invitation Fellowship for Research in Japan from the Japan Society for
the Promotion of Science.
*
Corresponding author; e-mail murata{at}nibb.ac.jp; fax
81-564-54-4866.
© 2001 American Society of Plant Physiologists
