4.8 Article

Response to substrate limitation by a marine sulfate-reducing bacterium

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ISME JOURNAL
卷 16, 期 1, 页码 200-210

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SPRINGERNATURE
DOI: 10.1038/s41396-021-01061-2

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资金

  1. Marie-Curie Individual Fellowship (DEEP CARBON FLUX) [327675]
  2. Danish National Research Foundation [DNRF104]
  3. European Research Council [ERC] [294200]
  4. Danish Council for Independent Research [DFF-7014-00196]

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The marine sulfate reducer Desulfobacterium autotrophicum adapts to substrate limitation through complete lactate oxidation and differential overexpression of genes involved in amino acid metabolism, and reroutes carbon metabolism in response to sulfate limitation. Upregulation of putative sulfate transporters suggests a key role of SRM in controlling sulfate concentration.
Sulfate-reducing microorganisms (SRM) in subsurface sediments live under constant substrate and energy limitation, yet little is known about how they adapt to this mode of life. We combined controlled chemostat cultivation and transcriptomics to examine how the marine sulfate reducer, Desulfobacterium autotrophicum, copes with substrate (sulfate or lactate) limitation. The half-saturation uptake constant (K-m) for lactate was 1.2 mu M, which is the first value reported for a marine SRM, while the K-m for sulfate was 3 mu M. The measured residual lactate concentration in our experiments matched values observed in situ in marine sediments, supporting a key role of SRM in the control of lactate concentrations. Lactate limitation resulted in complete lactate oxidation via the Wood-Ljungdahl pathway and differential overexpression of genes involved in uptake and metabolism of amino acids as an alternative carbon source. D. autotrophicum switched to incomplete lactate oxidation, rerouting carbon metabolism in response to sulfate limitation. The estimated free energy was significantly lower during sulfate limitation (-28 to -33 kJ mol(-1) sulfate), suggesting that the observed metabolic switch is under thermodynamic control. Furthermore, we detected the upregulation of putative sulfate transporters involved in either high or low affinity uptake in response to low or high sulfate concentration.

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