Cyanobacteria are widely distributed photosynthetic organism. During the day they store carbon, mainly as glycogen, to provide the energy and carbon source required for maintenance during the night. In this work we generate a mutant strain of the freshwater cyanobacterium Synechocystis sp. PCC 6803 lacking both glycogen synthases. This mutant presents a lethal phenotype due to massive accumulation of ADP-Glucose, the substrate of glycogen synthases. This accumulation leads to alterations in its photosynthetic capacity and dramatic decrease in the adenylate energy charge of the cell to values as low as 0.1. Lacking of ADP-Glucose pyrophosphorylase, the enzyme responsible of ADP-Glucose synthesis, or reintroduction of any of the glycogen synthases abolishes the lethal phenotype. In addition, viability of the glycogen synthases mutant is also fully recovered in NaCl-supplemented media, which redirects the surplus of ADP-Glucose to synthesize the osmolite glucosylglycerol. This alternative metabolic sink also suppresses phenotypes associated to the defective response to nitrogen deprivation characteristic of glycogen-less mutants, restoring the capacity of phycobiliproteins degradation. Thus, our system is an excellent example of how an inadequate management of the adenine nucleotide pools results in a lethal phenotype and the influence of metabolic carbon flux in cell viability and fitness.

中文翻译：

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在蓝细菌中，盐诱导的碳通量重定向会抑制ADP-葡萄糖积累引起的致命性。

蓝细菌是广泛分布的光合生物。在白天，它们存储碳，主要是作为糖原，以提供夜间维护所需的能量和碳源。在这项工作中，我们产生了淡水蓝藻集胞藻属（Synechocystis sp。）的突变株。缺少两种糖原合酶的PCC 6803。由于ADP-葡萄糖（糖原合酶的底物）的大量积累，此突变体呈现致死表型。这种积累导致其光合作用能力发生变化，并使细胞的腺苷酸能电荷急剧降低至低至0.1。缺乏引起ADP-葡萄糖合成的酶或重新引入任何糖原合酶的ADP-葡萄糖焦磷酸化酶消除了致死表型。此外，糖原合酶突变体的生存力也可以在添加了NaCl的培养基中完全回收，这会将多余的ADP-葡萄糖重新定向以合成渗透压葡萄糖基甘油。这种替代性代谢沉陷也抑制了与对无糖原突变体对氮缺乏特征的不良反应相关的表型，恢复了藻胆蛋白降解的能力。因此，我们的系统是一个很好的例子，说明腺嘌呤核苷酸池管理不当如何导致致命的表型以及代谢碳通量对细胞活力和适应性的影响。这种替代性代谢沉陷也抑制了与对无糖原突变体对氮缺乏特征的不良反应相关的表型，恢复了藻胆蛋白降解的能力。因此，我们的系统是一个很好的例子，说明腺嘌呤核苷酸池管理不当如何导致致命的表型以及代谢碳通量对细胞活力和适应性的影响。这种替代性代谢沉陷也抑制了与对无糖原突变体对氮缺乏特征的不良反应相关的表型，恢复了藻胆蛋白降解的能力。因此，我们的系统是一个很好的例子，说明腺嘌呤核苷酸池管理不当如何导致致命的表型以及代谢碳通量对细胞活力和适应性的影响。