Mironov Kirill S, Sidorov Roman A, Trofimova Marina S, Bedbenov Vladimir S, Tsydendambaev Vladimir D, Allakhverdiev Suleyman I, Los Dmitry A
Russian Academy of Sciences, Moscow, Russia.
Biochim Biophys Acta. 2012 Aug;1817(8):1352-9. doi: 10.1016/j.bbabio.2011.12.011. Epub 2011 Dec 27.
Cold stress causes unsaturation of the membrane lipids. This leads to adjustment of the membrane fluidity, which is necessary for cold acclimation of cells. Here we demonstrate that the cold-induced accumulation of PUFAs in the cyanobacterium Synechocystis is light-dependent. The desA(-)/desD(-) mutant, that lacks the genes for Δ12 and Δ6 desaturases, is still able to adjust the fluidity of its membranes in spite of its inability to synthesize PUFAs and modulate the fatty acid composition of the membrane lipids under cold stress. The expression of cold-induced genes, which are controlled by the cold sensor histidine kinase Hik33, depends on the fluidity of cell membranes and it is regulated by light, though it does not require the activity of the photosynthetic apparatus. The expression of cold-induced genes, which are not controlled by Hik33, does not depend on the membrane fluidity or light. Thus, membrane fluidity determines the temperature dependence of the expression of cold-induced genes that are under control of the Hik33, which might be the sensor of changes in the membrane fluidity. This article is part of a Special Issue entitled: Photosynthesis Research for Sustainability: from Natural to Artificial.
冷胁迫会导致膜脂不饱和。这会引起膜流动性的调整,而这对于细胞的冷驯化是必要的。在此我们证明,蓝藻集胞藻中多不饱和脂肪酸(PUFAs)的冷诱导积累是光依赖性的。desA(-)/desD(-)突变体缺乏Δ12和Δ6去饱和酶的基因,尽管其在冷胁迫下无法合成PUFAs并调节膜脂的脂肪酸组成,但仍能够调节其膜的流动性。由冷感受器组氨酸激酶Hik33控制的冷诱导基因的表达取决于细胞膜的流动性,并且受光调节,尽管它不需要光合装置的活性。不受Hik33控制的冷诱导基因的表达不依赖于膜流动性或光。因此,膜流动性决定了受Hik33控制的冷诱导基因表达的温度依赖性,Hik33可能是膜流动性变化的感受器。本文是名为“光合作用研究促进可持续发展:从自然到人工”的特刊的一部分。