Analysis and Redesign of Biological Networks Group, Max Planck Institute for Dynamics of Complex Technical Systems, Magdeburg, Germany.
FEBS J. 2012 Sep;279(18):3449-61. doi: 10.1111/j.1742-4658.2012.08520.x. Epub 2012 Mar 16.
Purple bacteria derive energy from aerobic respiration or photosynthesis depending on the availability of oxygen and light. Under aerobic conditions, photosynthesis genes are specifically repressed by the PpsR protein. In Rhodobacter sphaeroides, the repressive action of PpsR is antagonized by the blue-light and redox-sensitive flavoprotein AppA, which sequesters PpsR under anaerobic conditions into transcriptionally inactive complexes. However, under semi-aerobic conditions, blue-light excitation of AppA causes the AppA-PpsR complexes to dissociate, again leading to a repression of photosynthesis genes. We have recently developed a simple mathematical model suggesting that this phenotype arises from the formation of a maximum in the response curve of reduced PpsR at intermediate oxygen concentrations. However, this model focused mainly on the oxygen-dependent interactions whereas light regulation was only implemented in a simplified manner. In the present study, we incorporate a more detailed mechanism for the light-dependent interaction between AppA and PpsR, which now allows for a direct comparison with experiments. Specifically, we take into account that, upon blue-light excitation, AppA undergoes a conformational change, creating a long-lived signalling state causing the dissociation of the AppA-PpsR complexes. The predictions of the extended model are found to be in good agreement with experimental results on the light-dependent repression of photosynthesis genes under semi-aerobic conditions. We also identify the potential kinetic and stoichiometric constraints that the interplay between light and redox regulation imposes on the functionality of the AppA/PpsR system, especially with respect to a possible bistable response.
紫色细菌可以通过需氧呼吸或光合作用来获取能量，具体取决于氧气和光的可用性。在需氧条件下，光合作用基因会被 PpsR 蛋白特异性抑制。在球形红杆菌中，PpsR 的抑制作用会被蓝光和氧化还原敏感的黄素蛋白 AppA 拮抗，AppA 在厌氧条件下将 PpsR 隔离到转录不活跃的复合物中。然而，在半需氧条件下，蓝光激发 AppA 会导致 AppA-PpsR 复合物解离，再次导致光合作用基因的抑制。我们最近开发了一个简单的数学模型，表明这种表型是由于还原型 PpsR 在中间氧浓度下的响应曲线形成最大值而产生的。然而，该模型主要集中在氧依赖性相互作用上，而光调节只是以简化的方式实现。在本研究中，我们将 AppA 和 PpsR 之间的光依赖性相互作用的机制更加详细化，现在可以与实验进行直接比较。具体来说，我们考虑到，在蓝光激发下，AppA 会发生构象变化，形成一个长寿命的信号状态，导致 AppA-PpsR 复合物的解离。扩展模型的预测与半需氧条件下光合作用基因的光依赖性抑制的实验结果非常吻合。我们还确定了光和氧化还原调节之间相互作用对 AppA/PpsR 系统功能施加的潜在动力学和化学计量约束，特别是关于可能的双稳态响应。
