AME 82:129-144 (2018)  -  DOI: https://doi.org/10.3354/ame01887

ABSTRACT: Biodegradation is the most effective way to transform hepatotoxic microcystins produced by cyanobacteria in natural environments. An increasing number of new bacterial strains capable of microcystin degradation are being discovered, and there is still only one fully described metabolic pathway responsible for degradation, encoded by the mlr gene cluster. We aimed to identify microcystin-degrading bacteria in assemblages from water and bottom sediment of the eutrophic freshwater Lake Mikolajskie, Poland. Bacteria from water and sediment differed in taxonomic composition, and only in the community from sediment was the mlrA gene detected. In the presence of microcystins, bacteria from the sediment showed higher proteolytic activity, while in the water community, there was no change in the activity of proteases. Bacterial assemblages from both environments also showed different time profiles of microcystin utilization. All these results indicate that other metabolic pathways may be involved in the degradation of microcystins by bacteria living in the water and bottom sediment. Identified microcystin-degrading and potentially microcystin-degrading bacteria belong to Betaproteobacteria (genera: Hydrogenophaga, Comamonas, Rhodoferax) and Gammaproteobacteria (genera: Acinetobacter, Citrobacter, Rahnella, Serratia, Pseudomonas, Stenotrophomonas), according to denaturing gradient gel electrophoresis analysis, as well as isolation and testing of the properties of individual strains. No bacteria belonging to family Sphingomonadaceae (Alphaproteobacteria) were identified, which, until recently, were considered to be the main microcystin degraders. Several bacterial taxa detected in this study have never been previously described as potential microcystin degraders: Comamonas sp., Hydrogenophaga sp., Rhodoferax sp., Citrobacter sp., and Serratia sp.

KEY WORDS: Microcystins · Biodegradation · Betaproteobacteria · Gammaproteobacteria · Degradation pathway · mlrA gene