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Life on N2O: deciphering the ecophysiology of N2O respiring bacterial communities in a continuous culture
Reduction of the greenhouse gas N 2 O to N 2 is a trait among denitrifying and non-denitrifying microorganisms having an N 2 O reductase, encoded by nosZ . The nosZ phylogeny has two major clades, I and II, and physiological differences among organisms within the clades may affect N 2 O emissions fr...
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Published in: | The ISME Journal 2018-04, Vol.12 (4), p.1142-1153 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Reduction of the greenhouse gas N
2
O to N
2
is a trait among denitrifying and non-denitrifying microorganisms having an N
2
O reductase, encoded by
nosZ
. The
nosZ
phylogeny has two major clades, I and II, and physiological differences among organisms within the clades may affect N
2
O emissions from ecosystems. To increase our understanding of the ecophysiology of N
2
O reducers, we determined the thermodynamic growth efficiency of N
2
O reduction and the selection of N
2
O reducers under N
2
O- or acetate-limiting conditions in a continuous culture enriched from a natural community with N
2
O as electron acceptor and acetate as electron donor. The biomass yields were higher during N
2
O limitation, irrespective of dilution rate and community composition. The former was corroborated in a continuous culture of
Pseudomonas stutzeri
and was potentially due to cytotoxic effects of surplus N
2
O. Denitrifiers were favored over non-denitrifying N
2
O reducers under all conditions and Proteobacteria harboring clade I
nosZ
dominated. The abundance of
nosZ
clade II increased when allowing for lower growth rates, but bacteria with
nosZ
clade I had a higher affinity for N
2
O, as defined by
μ
max
/
K
s
. Thus, the specific growth rate is likely a key factor determining the composition of communities living on N
2
O respiration under growth-limited conditions. |
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ISSN: | 1751-7362 1751-7370 1751-7370 |
DOI: | 10.1038/s41396-018-0063-7 |