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微囊藻毒素-LR 结合铁,而铁促进其自组装。

Microcystin-LR Binds Iron, and Iron Promotes Self-Assembly.

机构信息

Institute for Biocomputation and Physics of Complex Systems (BIFI)-Joint Unit BIFI-IQFR (CSIC) , Aragón 50018, Spain.

出版信息

Environ Sci Technol. 2017 May 2;51(9):4841-4850. doi: 10.1021/acs.est.6b05939. Epub 2017 Apr 17.

DOI:10.1021/acs.est.6b05939
PMID:28368104
Abstract

The microcystin-producing Microcystis aeruginosa PCC 7806 and its close strain, the nonproducing Microcystis aeruginosa PCC 7005, grow similarly in the presence of 17 μM iron. Under severe iron deficient conditions (0.05 μM), the toxigenic strain grows slightly less than in iron-replete conditions, while the nonproducing microcystin strain is not able to grow. Isothermal titration calorimetry performed at cyanobacterial cytosol or meaningful environmental pHs values shows a microcystin-LR dissociaton constant for Fe and Fe of 2.4 μM. Using atomic force microscopy, 40% of microcystin-LR dimers were observed, and the presence of iron promoted its oligomerization up to six units. Microcystin-LR binds also Mo, Cu, and Mn. Polymeric microcystin binding iron may be related with a toxic cell colony advantage, providing enhanced iron bioavailability and perhaps affecting the structure of the gelatinous sheath. Inside cells, with microcystin implicated in the fitness of the photosynthetic machinery under stress conditions, the toxin would be involved in avoiding metal-dependent Fenton reactions when photooxidation causes disassembly of the iron-rich photosystems. Additionally, it could be hypothesized that polymerization-depolymerization dynamics may be an additional signal that could trigger changes (for example, in the binding of microcystin to proteins).

摘要

产微囊藻毒素的铜绿微囊藻 PCC 7806 及其近缘株非产微囊藻毒素的铜绿微囊藻 PCC 7005 在 17 μM 铁存在的情况下生长相似。在严重缺铁条件(0.05 μM)下,产毒株的生长略低于铁充足条件,而非产微囊藻毒素株则无法生长。在蓝细菌胞质溶胶或有意义的环境 pH 值下进行的等温滴定量热法显示,微囊藻毒素-LR 与 Fe 和 Fe 的解离常数为 2.4 μM。使用原子力显微镜观察到 40%的微囊藻毒素-LR 二聚体,并且铁的存在促进了其寡聚化至六个单位。微囊藻毒素-LR 还结合 Mo、Cu 和 Mn。多聚微囊藻毒素结合铁可能与毒性细胞集落优势有关,提供增强的铁生物利用度,并且可能影响凝胶状鞘的结构。在细胞内,由于微囊藻毒素参与应激条件下光合作用机构的适应性,毒素可能会参与避免金属依赖性芬顿反应,当光氧化导致富含铁的光合作用系统解体时。此外,可以假设聚合-解聚动力学可能是另一个信号,可以触发变化(例如,微囊藻毒素与蛋白质的结合)。

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