MSU-DOE Plant Research Laboratory, Michigan State University, East Lansing, MI 48824.
Ocean and Earth Science, University of Southampton, SO14 3ZH Southampton, United Kingdom.
Proc Natl Acad Sci U S A. 2021 Mar 16;118(11). doi: 10.1073/pnas.2021523118.
Cyanobacteria must prevent imbalances between absorbed light energy (source) and the metabolic capacity (sink) to utilize it to protect their photosynthetic apparatus against damage. A number of photoprotective mechanisms assist in dissipating excess absorbed energy, including respiratory terminal oxidases and flavodiiron proteins, but inherently reduce photosynthetic efficiency. Recently, it has been hypothesized that some engineered metabolic pathways may improve photosynthetic performance by correcting source/sink imbalances. In the context of this subject, we explored the interconnectivity between endogenous electron valves, and the activation of one or more heterologous metabolic sinks. We coexpressed two heterologous metabolic pathways that have been previously shown to positively impact photosynthetic activity in cyanobacteria, a sucrose production pathway (consuming ATP and reductant) and a reductant-only consuming cytochrome P450. Sucrose export was associated with improved quantum yield of phtotosystem II (PSII) and enhanced electron transport chain flux, especially at lower illumination levels, while cytochrome P450 activity led to photosynthetic enhancements primarily observed under high light. Moreover, coexpression of these two heterologous sinks showed additive impacts on photosynthesis, indicating that neither sink alone was capable of utilizing the full "overcapacity" of the electron transport chain. We find that heterologous sinks may partially compensate for the loss of photosystem I (PSI) oxidizing mechanisms even under rapid illumination changes, although this compensation is incomplete. Our results provide support for the theory that heterologous metabolism can act as a photosynthetic sink and exhibit some overlapping functionality with photoprotective mechanisms, while potentially conserving energy within useful metabolic products that might otherwise be "lost."
蓝藻必须防止吸收的光能（源）与代谢能力（汇）之间的失衡，以利用光能来保护其光合器官免受损伤。许多光保护机制有助于耗散多余的吸收能量，包括呼吸末端氧化酶和黄素铁蛋白，但会降低光合作用效率。最近，有人假设，一些工程代谢途径可以通过纠正源/汇失衡来提高光合作用性能。在这个主题的背景下，我们探索了内源性电子阀之间的相互连接性，以及一个或多个异源代谢汇的激活。我们共表达了两种以前在蓝藻中被证明能积极影响光合作用的异源代谢途径，一种是蔗糖生产途径（消耗 ATP 和还原剂），另一种是仅消耗细胞色素 P450 的还原剂。蔗糖的外排与 PSII（光系统 II）量子产率的提高和电子传递链通量的增强有关，尤其是在较低的光照水平下，而细胞色素 P450 的活性主要在高光下导致光合作用的增强。此外，这两种异源汇的共表达对光合作用表现出累加影响，表明单独的任何一个汇都不能利用电子传递链的全部“过容量”。我们发现，异源汇可能部分补偿光系统 I（PSI）氧化机制的损失，即使在快速光照变化下，尽管这种补偿是不完全的。我们的结果为异源代谢可以作为光合作用汇的理论提供支持，并表现出与光保护机制的一些重叠功能，同时将能量保存在可能否则会“损失”的有用代谢产物中。
