Mironov Kirill S, Sinetova Maria A, Shumskaya Maria, Los Dmitry A
Department of Molecular Biosystems, K.A. Timiryazev Institute of Plant Physiology, Russian Academy of Sciences, Botanicheskaya street 35, 127276 Moscow, Russian.
Department of Biology, School of Natural Sciences, Kean University, 1000 Morris Ave, Union, NJ 07083, USA.
Life (Basel). 2019 Aug 20;9(3):67. doi: 10.3390/life9030067.
Systemic analysis of stress-induced transcription in the cyanobacterium sp. strain PCC 6803 identifies a number of genes as being induced in response to most abiotic stressors (heat, osmotic, saline, acid stress, strong light, and ultraviolet radiation). Genes for heat-shock proteins (HSPs) are activated by all these stresses and form a group that universally responds to all environmental changes. The functions of universal triggers of stress responses in cyanobacteria can be performed by reactive oxygen species (ROS), in particular HO, as well as changes in the redox potential of the components of the photosynthetic electron transport chain. The double mutant of sp. PCC 6803 (, or ), which is defective in antioxidant enzymes catalase (KatG) and thioredoxin peroxidase (Tpx), cannot grow in the presence of exogenous hydrogen peroxide (HO); and it is extremely sensitive to low concentrations of HO, especially under conditions of cold stress. Experiments on this mutant demonstrate that HO is involved in regulation of gene expression that responds to a decrease in ambient temperature, and affects both the perception and the signal transduction of cold stress. In addition, they suggest that formation of ROS largely depends on the physical state of the membranes such as fluidity or viscosity. In cyanobacteria, an increase in membrane turnover leads to a decrease in the formation of ROS and an increase in resistance to cold stress. Therefore: (1) HO is the universal trigger of stress responses in cyanobacterial cells; (2) ROS formation (in particular, HO) depends on the physical properties of both cytoplasmic and thylakoid membranes; (3) The destructive effect of HO is reduced by increasing of fluidity of biological membranes.
对蓝藻菌株PCC 6803中应激诱导转录的系统分析确定了许多基因在响应大多数非生物应激源(热、渗透、盐、酸胁迫、强光和紫外线辐射)时被诱导。热休克蛋白(HSP)基因在所有这些胁迫下均被激活,并形成一组对所有环境变化都有普遍响应的基因。蓝藻中应激反应的通用触发因子的功能可以由活性氧(ROS),特别是羟基自由基(HO)以及光合电子传递链成分的氧化还原电位变化来执行。蓝藻菌株PCC 6803的双突变体(,或)在抗氧化酶过氧化氢酶(KatG)和硫氧还蛋白过氧化物酶(Tpx)方面存在缺陷,在外源过氧化氢(HO)存在的情况下无法生长;并且它对低浓度的HO极其敏感,尤其是在冷胁迫条件下。对该突变体的实验表明,HO参与了对环境温度降低作出响应的基因表达调控,并影响冷胁迫的感知和信号转导。此外,这些实验表明ROS的形成在很大程度上取决于膜的物理状态,如流动性或粘度。在蓝藻中,膜更新的增加会导致ROS形成减少以及对冷胁迫的抗性增加。因此:(1)HO是蓝藻细胞应激反应的通用触发因子;(2)ROS的形成(特别是HO)取决于细胞质膜和类囊体膜的物理性质;(3)通过增加生物膜的流动性可以降低HO的破坏作用。