The role of activated acetate intermediates in the control of biofilm amounts.

A previous study postulated that acetate metabolism was a metabolic sensory mechanism that related information about 's environment to the formation of biofilms (Prüβ et al., Arch. Microbiol. 2010). Considering that mutants in (no acetyl phosphate) and (high acetyl phosphate) exhibited similarly increased biofilm amounts and three dimensional structures, the hypothesis for this study was that acetyl Co-A was a more likely mediator of the acetate effect than acetyl phosphate. The effect of acetate metabolism on biofilm amounts was detailed by using single carbon sources rather than the previously used mixed amino acid medium, as well as mutations in additional genes that contribute to acetate metabolism (, , ). In summary, the mutations in and increased biofilm amounts in the presence of maltose, D-trehalose, D-mannose, and L-rhamnose, all of which get converted to acetyl-CoA. The mutant also exhibited increased biofilm amounts in the presence of inosine and thymidine. The mutation in decreased biofilm amounts in the presence of maltotriose, uridine, D-serine, and acetate. Since , , and mutants are expected to exhibit increased intracellular acetyl-CoA levels, and and mutants likely exhibit decreased acetyl-CoA concentrations, we believe that acetyl-CoA is the activated acetate intermediate that controls biofilm amounts.