文献类型：期刊文献

英文题名：Increasing NADPH impairs fungal H2O2 resistance by perturbing transcriptional regulation of peroxiredoxin

作者：Li, Jingyi[1];Sun, Yanwei[1];Liu, Feiyun[1];Zhou, Yao[1];Yan, Yunfeng[1];Zhou, Zhemin[2];Wang, Ping[3];Zhou, Shengmin[1]

机构：[1]East China Univ Sci & Technol, Sch Biotechnol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China;[2]Jiangnan Univ, Key Lab Ind Biotechnol, Minist Educ, Sch Biotechnol, 1800 Lihu Ave, Wuxi 214122, Jiangsu, Peoples R China;[3]Univ Minnesota, Dept Bioprod & Biosyst Engn, St Paul, MN 55108 USA

年份：2022

卷号：9

期号：1

外文期刊名：BIORESOURCES AND BIOPROCESSING

收录：;EI(收录号：20224513085996);WOS:【SCI-EXPANDED(收录号:WOS:000737920100001)】；

基金：This study was supported by the International S&T Innovation Cooperation Key Project (2017YFE0129600), the National Natural Science Foundation of China (21672065, 22077032 and 21636003), the National Major Science and Technology Projects of China (2019ZX09739001), the Fundamental Research Funds for the Central Universities (22221818014), and the 111 Project (B18022).

语种：英文

外文关键词：Peroxiredoxin; NADPH; Oxidative stress; Aspergillus; Glucose-6-phosphate dehydrogenase; AnCF

摘要：NADPH provides the reducing power for decomposition of reactive oxygen species (ROS), making it an indispensable part during ROS defense. It remains uncertain, however, if living cells respond to the ROS challenge with an elevated intracellular NADPH level or a more complex NADPH-mediated manner. Herein, we employed a model fungus Aspergillus nidulans to probe this issue. A conditional expression of glucose-6-phosphate dehydrogenase (G6PD)-strain was constructed to manipulate intracellular NADPH levels. As expected, turning down the cellular NADPH concentration drastically lowered the ROS response of the strain; it was interesting to note that increasing NADPH levels also impaired fungal H2O2 resistance. Further analysis showed that excess NADPH promoted the assembly of the CCAAT-binding factor AnCF, which in turn suppressed NapA, a transcriptional activator of PrxA (the key NADPH-dependent ROS scavenger), leading to low antioxidant ability. In natural cell response to oxidative stress, we noticed that the intracellular NADPH level fluctuated "down then up" in the presence of H2O2. This might be the result of a co-action of the PrxA-dependent NADPH consumption and NADPH-dependent feedback of G6PD. The fluctuation of NADPH is well correlated to the formation of AnCF assembly and expression of NapA, thus modulating the ROS defense. Our research elucidated how A. nidulans precisely controls NADPH levels for ROS defense.