The role of the bacterial cell surface and extracellular macromolecules in U(VI) biosorption and biomineralisation

• Main Author: Hufton, Joseph
• Other Authors: Romero-Gonzalez, Maria ; Harding, John
• Published: University of Sheffield 2016
• Subjects: 572
• Online Access: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.690157

Uranium biosorption and biomineralisation are processes exhibited by bacteria that aren’t fully understood at a mechanistic level, making it difficult to consider their use and application in remediation, extraction and reuse. The aim of this study was, therefore, to deconstruct the bacterial cell and characterise the specific roles of cell surface structures and extra polymeric substances, in order to elucidate their contribution to the biosorption and biomineralisation of uranium within live cells. The complexation and precipitation of uranium with extracellular DNA (eDNA) was predominantly mediated by negatively charged phosphate moieties within eDNA. The reaction was dependent on pH, where the formation of a precipitate was reduced as the pH increased. Towards circumneutral pH, acid phosphatase liberated phosphate from eDNA that precipitated uranium as a phosphate-bearing mineral. The biosorption of uranium with bacteria is governed by the interactions with functional groups at the cell surface. The cell wall isolates and lysed cells of B. subtilis 168 exhibited a greater uranium retention capacity in comparison to those from P. putida 33015, live cells and cell membrane isolates from both strains. Carboxyl groups and phosphate groups, from proteins and phosphorylated biopolymers, were responsible uranium biosorption with the cell surface structures. The viability and metabolic activity of live cells of P. putida 33015 and D. radiodurans R1 in the presence of uranium was evaluated. An increase in uranium concentration was directly linked to cell toxicity in both strains. At low concentrations of U(VI) and circumneutral pH, viable cells likely sequestered uranium either through biosorption or through the precipitation of enzymatically generated uranium phosphate minerals that were tethered to the cell surface or within EPS as a tolerance mechanism to cope with uranium toxicity. At higher concentrations of uranium or at low pH where the bacterial growth wasn’t favourable or there was cell death, biosorption to the bacterial biomass present likely occurred.