4.8 Article

Metabolism perturbation Caused by the overexpression of carbon monoxide dehydrogenase/Acetyl-CoA synthase gene complex accelerated gas to acetate conversion rate of Eubacterium limosum KIST612

Journal

BIORESOURCE TECHNOLOGY
Volume 341, Issue -, Pages -

Publisher

ELSEVIER SCI LTD
DOI: 10.1016/j.biortech.2021.125879

Keywords

Acetogen; Eubacterium limosum; CO dehydrogenase; Homologous overexpression; Metabolic change

Funding

  1. National Research Foundation of Korea (NRF) - Korean Government [2021R1A5A1028138]
  2. NRF - Ministry of Science and ICT [2021M3D3A1A01079730]
  3. Korea Institute of Energy Technology Evaluation and Planning - Ministry of Trade, Industry and Energy [20173010092460]
  4. Korea Evaluation Institute of Industrial Technology (KEIT) [20173010092460] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Through in silico prediction and in vivo assessment, we have successfully improved the rates of carbon monoxide conversion to acetate by Eubacterium limosum KIST612 strain.
Microbial conversion of carbon monoxide (CO) to acetate is a promising upcycling strategy for carbon sequestration. Herein, we demonstrate that CO conversion and acetate production rates of Eubacterium limosum KIST612 strain can be improved by in silico prediction and in vivo assessment. The mimicked CO metabolic model of KIST612 predicted that overexpressing the CO dehydrogenase (CODH) increases CO conversion and acetate production rates. To validate the prediction, we constructed mutant strains overexpressing CODH gene cluster and measured their CO conversion and acetate production rates. A mutant strain (ELM031) co-overexpressing CODH, coenzyme CooC2 and ACS showed a 3.1 x increased specific CO oxidation rate as well as 1.4 x increased specific acetate production rate, compared to the wild type strain. The transcriptional and translational data with redox balance analysis showed that ELM031 has enhanced reducing potential from up-regulation of ferredoxin and related metabolism directly linked to energy conservation.

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