Responses of AOA and AOB activity and DNA/cDNA community structure to allylthiourea exposure in the water level fluctuation zone soil
Ammonia oxidation is mainly performed by ammonia-oxidizing archaea (AOA) and ammonia-oxidizing bacteria (AOB). Allylthiourea (ATU) has been found to specifically inhibit ammonia oxidation. However, the effect of ATU on AOA and AOB transcription has been infrequently studied. In the present study, we...
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Veröffentlicht in: | Environmental science and pollution research international 2020-05, Vol.27 (13), p.15233-15244 |
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Sprache: | eng |
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Zusammenfassung: | Ammonia oxidation is mainly performed by ammonia-oxidizing archaea (AOA) and ammonia-oxidizing bacteria (AOB). Allylthiourea (ATU) has been found to specifically inhibit ammonia oxidation. However, the effect of ATU on AOA and AOB transcription has been infrequently studied. In the present study, we examined the responses of AOA and AOB activity and DNA/cDNA community structure to ATU exposure. The ammonia oxidation activity in the 100-mg/L ATU group was 4.3% of that in the control group after 7 days. When exposed to ATU, the gene abundance of AOA was favored compared with that of AOB, and there were no statistically significant differences in the abundance of AOB
amoA
in DNA and cDNA between the two groups. Compared with the control group, the gene abundance of AOA significantly increased by 5.23 times, while the transcription of AOA significantly decreased by 0.70 times. Moreover, the transcriptional ratio of AOA in the ATU group was only 0.05 times as high as that in the control group. ATU selectively affected AOB and completely inhibited
Nitrosomonas europaea
and
Bacterium amoA.22.HaldeII.kultur
at the genetic level. Under ATU exposure, all AOA clusters were transcribed, but three AOB clusters were not transcribed. Our results indicated that the ammonia oxidation potential of the soil of water level fluctuation areas, based on ATU inhibition, was associated mainly with AOA
amoA
gene abundance and AOB community shifts in DNA and cDNA. |
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ISSN: | 0944-1344 1614-7499 |
DOI: | 10.1007/s11356-020-07952-9 |