Here, we present a conceptual and quantitative model to describe the role of the Cytochrome \(\hbox {b}_{6}\hbox {f}\) complex in controlling steady-state electron transport in \(\hbox {C}_{3}\) leaves. The model is based on new experimental methods to diagnose the maximum activity of Cyt \(\hbox {b}_{6}\hbox {f}\) in vivo, and to identify conditions under which photosynthetic control of Cyt \(\hbox {b}_{6}\hbox {f}\) is active or relaxed. With these approaches, we demonstrate that Cyt \(\hbox {b}_{6}\hbox {f}\) controls the trade-off between the speed and efficiency of electron transport under limiting light, and functions as a metabolic switch that transfers control to carbon metabolism under saturating light. We also present evidence that the onset of photosynthetic control of Cyt \(\hbox {b}_{6}\hbox {f}\) occurs within milliseconds of exposure to saturating light, much more quickly than the induction of non-photochemical quenching. We propose that photosynthetic control is the primary means of photoprotection and functions to manage excitation pressure, whereas non-photochemical quenching functions to manage excitation balance. We use these findings to extend the Farquhar et al. (Planta 149:78–90, 1980) model of \(\hbox {C}_{3}\) photosynthesis to include a mechanistic description of the electron transport system. This framework relates the light captured by PS I and PS II to the energy and mass fluxes linking the photoacts with Cyt \(\hbox {b}_{6}\hbox {f}\), the ATP synthase, and Rubisco. It enables quantitative interpretation of pulse-amplitude modulated fluorometry and gas-exchange measurements, providing a new basis for analyzing how the electron transport system coordinates the supply of Fd, NADPH, and ATP with the dynamic demands of carbon metabolism, how efficient use of light is achieved under limiting light, and how photoprotection is achieved under saturating light. The model is designed to support forward as well as inverse applications. It can either be used in a stand-alone mode at the leaf-level or coupled to other models that resolve finer-scale or coarser-scale phenomena.

在这里，我们提出了一个概念和定量模型来描述细胞色素\(\hbox {b}_{6}\hbox {f}\)复合物在控制\(\hbox {C}中的稳态电子传输中的作用_{3}\)离开。该模型基于新的实验方法来诊断体内 Cyt \(\hbox {b}_{6}\hbox {f}\)的最大活性，并确定 Cyt \(\hbox光合作用控制的条件{b}_{6}\hbox {f}\)是活跃的或放松的。通过这些方法，我们证明 Cyt \(\hbox {b}_{6}\hbox {f}\)控制限制光下电子传输速度和效率之间的权衡，并充当代谢开关将控制转移到饱和光下的碳代谢。我们还提供了证据表明 Cyt 的光合作用控制\(\hbox {b}_{6}\hbox {f}\)发生在暴露于饱和光的几毫秒内，比诱导非光化学猝灭要快得多。我们认为光合作用控制是光保护的主要手段，其功能是管理激发压力，而非光化学猝灭功能是管理激发平衡。我们利用这些发现来扩展 Farquhar 等人的研究。 (Planta 149:78–90, 1980) \(\hbox {C}_{3}\)光合作用模型，包括电子传输系统的机械描述。该框架将 PS I 和 PS II 捕获的光与连接光反应与 Cyt \(\hbox {b}_{6}\hbox {f}\) 、ATP 合酶和 Rubisco 的能量和质量通量联系起来。 它能够对脉冲幅度调制荧光测定和气体交换测量进行定量解释，为分析电子传输系统如何协调 Fd、NADPH 和 ATP 的供应与碳代谢的动态需求、如何有效利用光提供了新的基础。是在限制光下实现的，以及如何在饱和光下实现光保护。该模型旨在支持正向和逆向应用。它可以在叶级以独立模式使用，也可以与解决更精细尺度或更粗尺度现象的其他模型结合使用。