Allakhverdiev Suleyman I, Murata Norio
Institute of Basic Biological Problems, Russian Academy of Sciences, Pushchino, Moscow Region 142290, Russia.
Photosynth Res. 2008 Oct-Dec;98(1-3):529-39. doi: 10.1007/s11120-008-9334-x. Epub 2008 Aug 1.
Recent studies of responses of cyanobacterial cells to salt stress have revealed that the NaCl-induced decline in the photosynthetic activities of photosystems II and I involves rapid and slow changes. The rapid decreases in the activities of both photosystems, which occur within a few minutes, are reversible and are associated with osmotic effects, which induce the efflux of water from the cytosol through water channels and rapidly increase intracellular concentrations of salts. Slower decreases in activity, which occur within hours, are irreversible and are associated with ionic effects that are due to the influx of Na(+) and Cl(-) ions through K(+)(Na(+)) channels and, probably, Cl(-) channels, with resultant dissociation of extrinsic proteins from photosystems. In combination with light stress, salt stress significantly stimulates photoinhibition by inhibiting repair of photodamaged photosystem II. Tolerance of photosystems to salt stress can be enhanced by genetically engineered increases in the unsaturation of fatty acids in membrane lipids and by intracellular synthesis of compatible solutes, such as glucosylglycerol and glycinebetaine. In this review, we summarize recent progress in research on the effects of salt stress on photosynthesis in cyanobacteria.
近期关于蓝藻细胞对盐胁迫响应的研究表明,NaCl 诱导的光系统 II 和光系统 I 光合活性下降涉及快速和缓慢变化。两个光系统活性在几分钟内发生的快速下降是可逆的,且与渗透效应有关,渗透效应会导致水通过水通道从细胞质中流出,并迅速增加细胞内盐浓度。数小时内发生的较慢的活性下降是不可逆的,且与离子效应有关,离子效应是由于 Na(+)和 Cl(-)离子通过 K(+)(Na(+))通道以及可能的 Cl(-)通道流入,导致外在蛋白与光系统解离。与光胁迫相结合时,盐胁迫通过抑制光损伤的光系统 II 的修复而显著刺激光抑制。通过基因工程增加膜脂中脂肪酸的不饱和度以及细胞内合成相容性溶质(如葡糖基甘油和甘氨酸甜菜碱),可以提高光系统对盐胁迫的耐受性。在本综述中,我们总结了盐胁迫对蓝藻光合作用影响的研究最新进展。