A Novel Regulator Modulates Glucan Production, Cell Aggregation and Biofilm Formation in SK36.

is an early colonizer of tooth surfaces and a key player in plaque biofilm development. However, the mechanism of biofilm formation of is still unclear. Here, we showed that deletion of a transcription factor, , promotes cell aggregation and biofilm formation in SK36. Glucan, a polysaccharide synthesized from sucrose, was over-produced and aggregated in the biofilm of Δ, which was necessary for better biofilm formation ability of Δ. Quantitative RT-PCR demonstrated that was significantly up-regulated in Δ, which increased the productions of water-insoluble and water-soluble glucans. The ΔΔ double mutant decreased biofilm formation ability of Δ to a level similar like that of Δ. Interestingly, the biofilm of Δ had an increased tolerance to ampicillin treatment, which might be due to better biofilm formation ability through the mechanisms of cellular and glucan aggregation. RNA sequencing and quantitative RT-PCR revealed the modulation of a group of genes in Δ was mediated by activating the expression of , another -related biofilm formation regulator. Double deletion of and decreased biofilm formation ability to the phenotype of a Δ mutant. Additionally, RNA sequencing elucidated a broad range of genes, related to carbohydrate metabolism and uptake, were activated in Δ. SSA_0222, a gene involved in the phosphotransferase system, was dramatically up-regulated in Δ and essential for survival under our experimental conditions. In summary, modulates glucan production, cell aggregation and biofilm formation by regulating the expression of in SK36.