Maksimov Eugene G, Mironov Kirill S, Trofimova Marina S, Nechaeva Natalya L, Todorenko Daria A, Klementiev Konstantin E, Tsoraev Georgy V, Tyutyaev Eugene V, Zorina Anna A, Feduraev Pavel V, Allakhverdiev Suleyman I, Paschenko Vladimir Z, Los Dmitry A
Department of Biophysics, Faculty of Biology, M.V. Lomonosov Moscow State University, Moscow, Russia, 119992.
Timiryazev Institute of Plant Physiology, Russian Academy of Sciences, Moscow, Russia, 127276.
Photosynth Res. 2017 Sep;133(1-3):215-223. doi: 10.1007/s11120-017-0337-3. Epub 2017 Jan 21.
Membrane fluidity is the important regulator of cellular responses to changing ambient temperature. Bacteria perceive cold by the transmembrane histidine kinases that sense changes in thickness of the cytoplasmic membrane due to its rigidification. In the cyanobacterium Synechocystis, about a half of cold-responsive genes is controlled by the light-dependent transmembrane histidine kinase Hik33, which also partially controls the responses to osmotic, salt, and oxidative stress. This implies the existence of some universal, but yet unknown signal that triggers adaptive gene expression in response to various stressors. Here we selectively probed the components of photosynthetic machinery and functionally characterized the thermodynamics of cyanobacterial photosynthetic membranes with genetically altered fluidity. We show that the rate of oxidation of the quinone pool (PQ), which interacts with both photosynthetic and respiratory electron transport chains, depends on membrane fluidity. Inhibitor-induced stimulation of redox changes in PQ triggers cold-induced gene expression. Thus, the fluidity-dependent changes in the redox state of PQ may universally trigger cellular responses to stressors that affect membrane properties.
膜流动性是细胞对环境温度变化作出反应的重要调节因子。细菌通过跨膜组氨酸激酶感知寒冷，这些激酶能检测到由于细胞质膜硬化导致的膜厚度变化。在蓝藻集胞藻中，约一半的冷响应基因由光依赖型跨膜组氨酸激酶Hik33控制，该激酶也部分控制对渗透、盐和氧化应激的反应。这意味着存在某种通用但未知的信号，可触发针对各种应激源的适应性基因表达。在此，我们选择性地探究了光合机构的组成部分，并对具有基因改变流动性的蓝藻光合膜的热力学进行了功能表征。我们发现，与光合和呼吸电子传输链都相互作用的醌池（PQ）的氧化速率取决于膜流动性。抑制剂诱导的PQ氧化还原变化刺激会触发冷诱导基因表达。因此，PQ氧化还原状态的流动性依赖性变化可能普遍触发细胞对影响膜特性的应激源的反应。
