4.6 Article

Redox interference in nitrogen status via oxidative stress is mediated by 2-oxoglutarate in cyanobacteria

期刊

NEW PHYTOLOGIST
卷 224, 期 1, 页码 216-228

出版社

WILEY
DOI: 10.1111/nph.15979

关键词

2-oxoglutarate; cyanobacteria; glutamine synthetase; hydrogen peroxide (H2O2); nitrogen metabolism; oxidative stress; Synechocystis

资金

  1. Ministerio de Economia y Competitividad [BFU2013-41712, AP2010-0366]
  2. Agencia Estatal de Investigacion (AEI) [BIO2016-75634-P]
  3. Ministerio de Economia, Industria y Competitividad
  4. Junta de Andalucia [P12-BIO-1119]
  5. FEDER

向作者/读者索取更多资源

Reactive oxygen species (ROS) are generated naturally in photosynthetic organisms by respiration and photosynthesis. Therefore, detoxification of these compounds, avoiding oxidative stress, is essential for proper cell function. In cyanobacteria, some observations point to a crosstalk between ROS homeostasis, in particular hydrogen peroxide, and nitrogen metabolism by a mechanism independent of known redox regulators. Using glutamine synthetase (GS), a finely regulated enzyme essential for nitrogen assimilation, as a tool, we were able to monitor nitrogen metabolism in relation to oxidative stress. We show that hydrogen peroxide clearly alters the expression of different genes related to nitrogen metabolism, both in the wild-type strain of the cyanobacterium Synechocystis sp. PCC 6803 and in a mutant strain lacking the catalase-peroxidase encoded by the katG gene and therefore highly sensitive to oxidative stress. As cyanobacteria perceive nitrogen status by sensing intracellular 2-oxoglutarate (2-OG) concentrations, the hydrogen peroxide effect was analysed under different nitrogen conditions in the wild-type, the increment katG strain and in a strain able to transport 2-OG. The results obtained demonstrate that hydrogen peroxide interferes with signalling of cellular carbon : nitrogen status by decreasing the intracellular concentrations of 2-OG and hence altering the function of the 2-OG-sensing global nitrogen regulator NtcA.

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