Sodium Lactate Negatively Regulates Shewanella putrefaciens CN32 Biofilm Formation via a Three-Component Regulatory System (LrbS-LrbA-LrbR).

The capability of biofilm formation has a major impact on the industrial and biotechnological applications of CN32. However, the detailed regulatory mechanisms underlying biofilm formation in this strain remain largely unknown. In the present report, we describe a three-component regulatory system which negatively regulates the biofilm formation of CN32. This system consists of a histidine kinase LrbS (Sputcn32_0303) and two cognate response regulators, including a transcription factor, LrbA (Sputcn32_0304), and a phosphodiesterase, LrbR (Sputcn32_0305). LrbS responds to the signal of the carbon source sodium lactate and subsequently activates LrbA. The activated LrbA then promotes the expression of , the gene for the other response regulator. The bis-(3'-5')-cyclic dimeric GMP (c-di-GMP) phosphodiesterase LrbR, containing an EAL domain, decreases the concentration of intracellular c-di-GMP, thereby negatively regulating biofilm formation. In summary, the carbon source sodium lactate acts as a signal molecule that regulates biofilm formation via a three-component regulatory system (LrbS-LrbA-LrbR) in CN32. Biofilm formation is a significant capability used by some bacteria to survive in adverse environments. Numerous environmental factors can affect biofilm formation through different signal transduction pathways. Carbon sources are critical nutrients for bacterial growth, and their concentrations and types significantly influence the biomass and structure of biofilms. However, knowledge about the underlying mechanism of biofilm formation regulation by carbon source is still limited. This work elucidates a modulation pattern of biofilm formation negatively regulated by sodium lactate as a carbon source via a three-component regulatory system in CN32, which may serve as a good example for studying how the carbon sources impact biofilm development in other bacteria.