4.1 Article

Global transcriptional analysis of Escherichia coli expressing IrrE, a regulator from Deinococcus radiodurans, in response to NaCl shock

Journal

MOLECULAR BIOSYSTEMS
Volume 11, Issue 4, Pages 1165-1171

Publisher

ROYAL SOC CHEMISTRY
DOI: 10.1039/c5mb00080g

Keywords

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Funding

  1. National Natural Science Foundation of China [31170105, 31370126]
  2. National Basic Research (973) Program of China [2015CB755701]
  3. National High-Tech (863) Program of China [2012AA063503, 2012AA02A703]
  4. National Research and Development Project of Transgenic Crops of China [2014ZX0800301B-003]
  5. Special Fund for Agro-scientific Research in the Public Interest [201103007]

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Improving the microbial tolerance to stresses is very important for bioprocesses. Our previous study showed that IrrE, a global regulator from the extremely radioresistant bacterium Deinococcus radiodurans, dramatically enhanced the multi-stress tolerance of Escherichia coli when expressed exogenously. However, the function of IrrE is still unclear. In this study, we used whole-genome microarray assays to profile the global gene expression of the IrrE-expressing E. coli strain MGE and the control strain MGT with or without salt shock. The analysis showed that IrrE expression led to many differentially expressed genes in E. coli, which were responsible for the transport and metabolism of trehalose and glycerol, nucleotide biosynthesis, carbon source utilization, amino acid utilization, and acid resistance, including many RpoS-dependent genes, e.g., the trehalose biosynthesis genes otsAB, the acid-resistance genes gadABC and uspB, the osmotic and oxidative stress response genes katE (response to DNA damage stimulus and stress) and osmBC (response to stress), and gadWX (which controls the transcription of pH-inducible genes). The intracellular content of trehalose and glycerol increased significantly in the IrrE-expressing strain after NaCl treatment for 0 and 60 min as determined by HPLC. These results indicated the possibility that IrrE regulates the global regulator RpoS. Interestingly, we found that although IrrE did not affect the level of the rpoS transcript, it enhanced the accumulation of the RpoS protein by increasing the expression of the antiadaptors, AppY, IraM and IraD, which inhibit RpoS degradation, suggesting that the accumulation of RpoS due to IrrE regulation is an important way to improve tolerance to salt and other stresses in E. coli.

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