Glutamine synthetase mRNA releases sRNA from its 3′UTR to regulate carbon/nitrogen metabolic balance in Enterobacteriaceae

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  • Masatoshi Miyakoshi
    Department of Infection Biology, Faculty of Medicine, University of Tsukuba
  • Teppei Morita
    Institute for Advanced Biosciences, Keio University
  • Asaki Kobayashi
    Transborder Medical Research Center, University of Tsukuba
  • Anna Berger
    International Joint Degree Master’s Program in Agro-Biomedical Science in Food and Health (GIP-TRIAD), University of Tsukuba
  • Hiroki Takahashi
    Medical Mycology Research Center, Chiba University
  • Yasuhiro Gotoh
    Department of Bacteriology, Faculty of Medical Sciences, Kyushu University
  • Tetsuya Hayashi
    Department of Bacteriology, Faculty of Medical Sciences, Kyushu University
  • Kan Tanaka
    Laboratory for Chemistry and Life Science, Institute of Innovative Research, Tokyo Institute of Technology

説明

<jats:p>Glutamine synthetase (GS) is the key enzyme of nitrogen assimilation induced under nitrogen limiting conditions. The carbon skeleton of glutamate and glutamine, 2-oxoglutarate, is supplied from the TCA cycle, but how this metabolic flow is controlled in response to nitrogen availability remains unknown. We show that the expression of the E1o component of 2-oxoglutarate dehydrogenase, SucA, is repressed under nitrogen limitation in <jats:italic>Salmonella enterica</jats:italic> and <jats:italic>Escherichia coli</jats:italic>. The repression is exerted at the post-transcriptional level by an Hfq-dependent sRNA GlnZ generated from the 3′UTR of the GS-encoding <jats:italic>glnA</jats:italic> mRNA. Enterobacterial GlnZ variants contain a conserved seed sequence and primarily regulate <jats:italic>sucA</jats:italic> through base-pairing far upstream of the translation initiation region. During growth on glutamine as the nitrogen source, the <jats:italic>glnA</jats:italic> 3′UTR deletion mutants expressed SucA at higher levels than the <jats:italic>S. enterica</jats:italic> and <jats:italic>E. coli</jats:italic> wild-type strains, respectively. In <jats:italic>E. coli</jats:italic>, the transcriptional regulator Nac also participates in the repression of <jats:italic>sucA</jats:italic>. Lastly, this study clarifies that the release of GlnZ from the <jats:italic>glnA</jats:italic> mRNA by RNase E is essential for the post-transcriptional regulation of <jats:italic>sucA</jats:italic>. Thus, the mRNA coordinates the two independent functions to balance the supply and demand of the fundamental metabolites.</jats:p>

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  • eLife

    eLife 11 2022-11-28

    eLife Sciences Publications, Ltd

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