Upon a dark-to-light transition, multiple species of cyanobacteria release a certain amount of H⁺ from the inside to the outside of their cells. Previous studies revealed the plasma membrane-localizing Proton exchange A (PxcA) is involved in the light-induced H⁺ extrusion in the cyanobacterium Synechocystis sp. PCC6803. Among oxygenic phototrophs, two PxcA homologs are conserved; they are the nuclear-encoded Day-length-dependent delayed-greening1 (DLDG1) and the plastid-encoded Ycf10 in Arabidopsis thaliana. We previously identified the putative DLDG1/Ycf10-interacting protein, Fluctuating-light acclimation protein1 (FLAP1), required for pH regulation in Arabidopsis chloroplasts. Synechocystis has PxcA and FLAP1 homologs designated here as PxcA like (PxcL) and FLAP1 homolog A (FlpA). Synechocystis mutants lacking pxcA, pxcL, and flpA were constructed and characterized to gain more insight into regulatory mechanisms of light-induced H⁺ extrusion in cyanobacteria. pH change kinetics of the extracellular solvent after shifting Synechocystis cells from dark to light indicated that PxcA is essential for the light-induced H⁺ extrusion, and both PxcA and PxcL were involved in H⁺ uptake. Mutational loss of flpA resulted in altered PxcA- and PxcL-dependent H⁺ efflux/influx activities, and the flpA-null mutant showed inhibited growth under dark–light cycles, indicating the importance of FlpA function for photosynthetic growth under fluctuating light. Collectively, these data suggest that PxcA is involved in H⁺ efflux immediately after light irradiation for the rapid formation of the H⁺ concentration gradient across the thylakoid membranes, PxcL is involved in H⁺ influx for activation of the Calvin-Benson-Bassham cycle, and FlpA controls the H⁺ transport under fluctuating light.

在从暗到亮的过渡过程中，多种蓝细菌从其细胞的内部向外部释放一定量的H ⁺。先前的研究表明质膜本地化质子交换A（PxcA）参与了蓝藻集胞藻（Synechocystcystis sp。）中光诱导的H ⁺挤出。PCC6803。在含氧营养养分中，两个PxcA同源物是保守的。它们是拟南芥中核编码的依赖天长的延迟绿化1（DLDG1）和质体编码的Ycf10 。我们之前确定了拟南芥叶绿体中调节pH所需的假定的DLDG1 / Ycf10相互作用蛋白，起伏驯化蛋白1（FLAP1）。突囊藻具有在此称为PxcA（PxcL）和FLAP1同系物A（FlpA）的PxcA和FLAP1同系物。缺乏pxcA，pxcL和flpA的集胞藻突变体的构建和表征可以更深入地了解蓝细菌中光诱导的H ⁺挤出的调控机制。突囊藻细胞从黑暗转移到光亮后，细胞外溶剂的pH改变动力学表明PxcA对于光诱导的H ⁺挤出至关重要，并且PxcA和PxcL均参与了H ^+的吸收。flpA的突变丢失导致PxcA和PxcL依赖的H ⁺改变外排/流入活动，并且flpA- null突变体在暗光循环下显示出受抑制的生长，表明FlpA功能对于在波动的光下光合生长的重要性。总体而言，这些数据表明，在光照射后，PxcA立即参与了H ^+的流出，从而在整个类囊体膜上迅速形成了H ⁺浓度梯度； PxcL参与了H ^+的流入，从而激活了Calvin-Benson-Bassham循环， FlpA在波动的光线下控制H ^+的传输。