The present study shows the existence of P_II-acetyl-CoA carboxylase interaction in the cyanobacterium Synechococcus sp. PCC 7942 and the possible adverse impact of nitrogen starvation on this interaction. The in silico and in vitro analysis of P_II-acetyl-CoA carboxylase interaction revealed that the biotin carboxyl carrier protein subunit of acetyl-CoA carboxylase enzyme actually interacts with the T-loop of P_II protein. However, exposure of the cyanobacterium to nitrogen-starved condition showed a higher expression and activity of acetyl-CoA carboxylase at the intracellular level which denoted the impairment of P_II-acetyl-CoA carboxylase interaction. A similar stimulatory effect of nitrogen starvation has also been noticed in the P_II mutant of Synechococcus PCC 7942. Further, the physiological study reflected that nitrogen starvation–caused reactive oxygen species generation in the wild-type and P_II mutant strains and lipid was increased in both strains of Synechococcus sp. PCC 7942. Proteomic analysis showed the upregulation of glycogen synthase, biotin carboxylase, and antioxidative enzymes and the deregulation of proteins involved in photosynthesis, energy metabolism, and protein synthesis. Interestingly, enhanced accumulation of transcripts of few tricarboxylic acid cycle genes was also noticed in the wild type. Although oxidative stress and lipid production were enhanced in both the test strains under nitrogen starvation, the impacts were more prominent in the mutant strain. Our results suggest that the nitrogen starvation–induced oxidative stress possibly relieved the P_II-mediated inhibition of acetyl-CoA carboxylase and led to increased lipid synthesis in Synechococcus PCC 7942.

本研究表明在蓝细菌Synchococcus sp。中存在P _II-乙酰-CoA羧化酶相互作用。PCC 7942和氮饥饿对这种相互作用的可能不利影响。P _II-乙酰-CoA羧化酶相互作用的计算机和体外分析表明，乙酰-CoA羧化酶的生物素羧基载体蛋白亚基实际上与P _II蛋白的T-环相互作用。然而，将蓝细菌暴露于氮饥饿条件下，表明其在细胞内水平上具有较高的乙酰辅酶A羧化酶表达和活性，这表明P _II受损。-乙酰基-CoA羧化酶相互作用。Synechococcus PCC 7942的P _II突变体中也注意到了氮饥饿的类似刺激作用。此外，生理研究表明，野生型和P _II突变株和脂质中氮饥饿引起的活性氧生成增加了。在两种菌株聚球蓝细菌sp。PCC7942。蛋白质组学分析显示糖原合酶，生物素羧化酶和抗氧化酶的上调以及与光合作用，能量代谢和蛋白质合成有关的蛋白质的失调。有趣的是，在野生型中也观察到少量三羧酸循环基因的转录物的积累增加。尽管在氮饥饿下两个测试菌株中氧化应激和脂质产生均增加，但是在突变菌株中影响更为显着。我们的结果表明，氮饥饿引起的氧化应激可能缓解了P _II介导的对乙酰辅酶A羧化酶的抑制作用，并导致Synechococcu s PCC 7942中脂质合成的增加。