Alamethicin Suppresses Methanogenesis and Promotes Acetogenesis in Bioelectrochemical Systems
KAUST Grant NumberKUS-I1-003-13
Online Publication Date2015-03-27
Print Publication Date2015-06-01
Permanent link to this recordhttp://hdl.handle.net/10754/597484
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AbstractMicrobial electrosynthesis (MES) systems with mixed cultures often generate a variety of gaseous and soluble chemicals. Methane is the primary end product in mixed-culture MES because it is the thermodynamically most favorable reduction product of CO2. Here, we show that the peptaibol alamethicin selectively suppressed the growth of methanogens in mixed-culture MES systems, resulting in a shift of the solution and cathode communities to an acetate-producing system dominated by Sporomusa, a known acetogenic genus in MES systems. Archaea in the methane-producing control were dominated by Methanobrevibacter species, but no Archaea were detected in the alamethicin-treated reactors. No methane was detected in the mixed-culture reactors treated with alamethicin over 10 cycles (∼ 3 days each). Instead, acetate was produced at an average rate of 115 nmol ml(-1) day(-1), similar to the rate reported previously for pure cultures of Sporomusa ovata on biocathodes. Mixed-culture control reactors without alamethicin generated methane at nearly 100% coulombic recovery, and no acetate was detected. These results show that alamethicin is effective for the suppression of methanogen growth in MES systems and that its use enables the production of industrially relevant organic compounds by the inhibition of methanogenesis.
CitationZhu X, Siegert M, Yates MD, Logan BE (2015) Alamethicin Suppresses Methanogenesis and Promotes Acetogenesis in Bioelectrochemical Systems. Appl Environ Microbiol 81: 3863–3868. Available: http://dx.doi.org/10.1128/AEM.00594-15.
SponsorsThis research was supported by award KUS-I1-003-13 from the King Abdullah University of Science and Technology (KAUST) and the Global Climate and Energy Program (GCEP).
PublisherAmerican Society for Microbiology
PubMed Central IDPMC4421063
CollectionsPublications Acknowledging KAUST Support
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