Abstract
The luxS gene is present in a wide range of bacteria and is involved in many cellular processes. LuxS mutation can cause autoinducer(AI)-2 deficiency and methyl metabolism disorder. The objective of this study was to demonstrate that, in addition to AI-2-mediated quorum sensing (QS), methyl metabolism plays an important role in LuxS regulation in Streptococcus mutans. The sahH gene from Pseudomonas aeruginosa was amplified and introduced into the S. mutans luxS-null strain to complement the methyl metabolism disruption in a defective QS phenotype. The intracellular activated methyl cycle (AMC) metabolites [S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), homocysteine (HCY), and methionine] were quantified in wild-type S. mutans and its three derivatives to determine the metabolic effects of disrupting the AMC. Biofilm mass and structure, acid tolerance, acid production, exopolysaccharide synthesis of multispecies biofilms and the transcriptional level of related genes were determined. The results indicated that SAH and SAM were relatively higher in S. mutans luxS-null strain and S. mutans luxS null strain with plasmid pIB169 when cultured overnight, and HCY was significantly higher in S. mutans UA159. Consistent with the transcriptional profile, luxS deletion-mediated impairment of biofilm formation and acid tolerance was restored to wild-type levels using transgenic SahH. These results also suggest that methionine methyl metabolism contributes to LuxS regulation in S. mutans to a significant degree.
Highlights
Streptococcus mutans is naturally present in the human oral microbiota and is considered a primary etiological agent of caries, which is the most prevalent oral disease (Loesche, 1986; Ghasempour et al, 2013)
The amount of SAH and SAM was significantly higher in Sm. S. mutans luxSnull strain (luxS) and Sm. luxS/pIB169 strains than in their counterparts, and HCY was higher in Sm.wt (Figure 1C, P < 0.05)
The results suggested that complementation of S-adenosyl-L-homocysteine hydrolase (SahH) partially restored the activated methyl cycle (AMC) metabolism in S.mutans
Summary
Streptococcus mutans is naturally present in the human oral microbiota and is considered a primary etiological agent of caries, which is the most prevalent oral disease (Loesche, 1986; Ghasempour et al, 2013). Metabolism Contributes to luxS-Mutation Impairments methyl cycle (AMC; Figure 1A), which generates activated methyl groups for the methylation of DNA, RNA, and proteins (Winzer et al, 2002; Sun et al, 2004; Parveen and Cornell, 2011; Redanz et al, 2012). SAH is converted into homocysteine (HCY) through a two-step process. SAH uses the enzyme Pfs to generate S-ribosyl-homocysteine, converted into homocysteine (HCY) by the enzyme LuxS (Díaz et al, 2014). For bacteria without LuxS/Pfs pathway, including Pseudomonas aeruginosa, S-adenosyl-L-homocysteine hydrolase (SahH) encoded by sahH is used to complete the AMC (Cataldi et al, 2009; Fernandez-Sanchez et al, 2009). In contrast to the LuxS/Pfs-dependent two-step pathway, SahH directly catalyzes the toxic intermediate SAH into HCY without generating AI-2 (Wang et al, 2012)
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