Publication Date:
2016-04-07
Description:
Recently, it has been shown that procyanidins from Fallopia spp. inhibit bacterial denitrification, a phenomenon called biological denitrification inhibition (BDI). However, the mechanisms involved in such a process remain unknown. Here, we investigate the mechanisms of BDI involving procyanidins, using the model strain Pseudomonas brassicacearum NFM 421. The aerobic and anaerobic (denitrification) respiration, cell permeability and cell viability of P. brassicacearum were determined as a function of procyanidin concentration. The effect of procyanidins on the bacterial membrane was observed using transmission electronic microscopy. Bacterial growth, denitrification, NO 3 - and NO 2 -reductase activity, and the expression of subunits of NO 3 - (encoded by the gene narG ) and NO 2 -reductase (encoded by the gene nirS ) under NO 3 or NO 2 were measured with and without procyanidins. Procyanidins inhibited the denitrification process without affecting aerobic respiration at low concentrations. Procyanidins also disturbed cell membranes without affecting cell viability. They specifically inhibited NO 3 - but not NO 2 -reductase. Pseudomonas brassicacearum responded to procyanidins by over-expression of the membrane-bound NO 3 -reductase subunit (encoded by the gene narG ). Our results suggest that procyanidins can specifically inhibit membrane-bound NO 3 -reductase inducing enzymatic conformational changes through membrane disturbance and that P. brassicacearum responds by over-expressing membrane-bound NO 3 -reductase. Our results lead the way to a better understanding of BDI.
Print ISSN:
0168-6496
Electronic ISSN:
1574-6941
Topics:
Biology
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