Laboratory for Chemistry and Life Science, Institute for Innovative Research, Tokyo Institute of Technology, Nagatsuta 4259-R1-8, Midori-ku, Yokohama, 226-8503, Japan.
Department of Life Science, Tokyo Institute of Technology, Nagatsuta, Midori-ku, Yokohama, 226-8501, Japan.
J Biochem. 2021 Sep 7;169(6):709-719. doi: 10.1093/jb/mvab014.
To understand the physiological role of NADPH-thioredoxin reductase C (NTRC) in cyanobacteria, we investigated an NTRC-deficient mutant strain of Anabaena sp., PCC 7120, cultivated under different regimes of nitrogen supplementation and light exposure. The deletion of ntrC did not induce a change in the cell structure and metabolic pathways. However, time-dependent changes in the abundance of specific proteins and metabolites were observed. A decrease in chlorophyll a was correlated with a decrease in chlorophyll a biosynthesis enzymes and photosystem I subunits. The deletion of ntrC led to a deregulation of nitrogen metabolism, including the NtcA accumulation and heterocyst-specific proteins while nitrate ions were available in the culture medium. Interestingly, this deletion resulted in a redox imbalance, indicated by higher peroxide levels, higher catalase activity and the induction of chaperones such as MsrA. Surprisingly, the antioxidant protein 2-CysPrx was downregulated. The deficiency in ntrC also resulted in the accumulation of metabolites such as 6-phosphogluconate, ADP and ATP. Higher levels of NADP+ and NADPH partly correlated with higher G6PDH activity. Rather than impacting protein expression levels, NTRC appears to be involved in the direct regulation of enzymes, especially during the dark-to-light transition period.
为了了解 NADPH-硫氧还蛋白还原酶 C(NTRC)在蓝藻中的生理作用,我们研究了在不同氮补充和光照条件下培养的鱼腥藻 PCC 7120 的 NTRC 缺失突变株。ntrC 的缺失并没有引起细胞结构和代谢途径的改变。然而,观察到特定蛋白质和代谢物丰度的时变变化。叶绿素 a 的减少与叶绿素 a 生物合成酶和光系统 I 亚基的减少相关。ntrC 的缺失导致氮代谢的失调,包括 NtcA 的积累和异形胞特异性蛋白,而硝酸盐离子在培养基中可用。有趣的是,这种缺失导致了氧化还原失衡,表现为过氧化物水平升高、过氧化氢酶活性升高以及伴侣蛋白如 MsrA 的诱导。令人惊讶的是,抗氧化蛋白 2-CysPrx 下调。ntrC 的缺乏也导致了 6-磷酸葡萄糖酸、ADP 和 ATP 等代谢物的积累。NADP+和 NADPH 的水平升高与 G6PDH 活性升高部分相关。NTRC 似乎参与了酶的直接调节,而不是影响蛋白质表达水平,特别是在从暗到光的过渡期间。