Deficiency of PdxR in Streptococcus mutans affects vitamin B 6 metabolism, acid tolerance response and biofilm formation

Streptococcus mutans, a key etiological agent of the human dental caries, lives primarily on the tooth surface in tenacious biofilms. The SMU 864 locus, designated pdxR, is predicted to encode a member of the novel MocR/GabR family proteins, which are featured with a winged helix DNA ‐binding N‐term...

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Veröffentlicht in:Molecular oral microbiology 2015-08, Vol.30 (4), p.255-268
Hauptverfasser: Liao, S., Bitoun, J.P., Nguyen, A.H., Bozner, D., Yao, X., Wen, Z.T.
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container_end_page 268
container_issue 4
container_start_page 255
container_title Molecular oral microbiology
container_volume 30
creator Liao, S.
Bitoun, J.P.
Nguyen, A.H.
Bozner, D.
Yao, X.
Wen, Z.T.
description Streptococcus mutans, a key etiological agent of the human dental caries, lives primarily on the tooth surface in tenacious biofilms. The SMU 864 locus, designated pdxR, is predicted to encode a member of the novel MocR/GabR family proteins, which are featured with a winged helix DNA ‐binding N‐terminal domain and a C‐terminal domain highly homologous to the pyridoxal phosphate‐dependent aspartate aminotransferases. A pdxR ‐deficient mutant, TW 296, was constructed using allelic exchange. PdxR deficiency in S. mutans had little effect on cell morphology and growth when grown in brain heart infusion. However, when compared with its parent strain, UA 159, the PdxR ‐ deficient mutant displayed major defects in acid tolerance response and formed significantly fewer biofilms ( P 
doi_str_mv 10.1111/omi.12090
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The SMU 864 locus, designated pdxR, is predicted to encode a member of the novel MocR/GabR family proteins, which are featured with a winged helix DNA ‐binding N‐terminal domain and a C‐terminal domain highly homologous to the pyridoxal phosphate‐dependent aspartate aminotransferases. A pdxR ‐deficient mutant, TW 296, was constructed using allelic exchange. PdxR deficiency in S. mutans had little effect on cell morphology and growth when grown in brain heart infusion. However, when compared with its parent strain, UA 159, the PdxR ‐ deficient mutant displayed major defects in acid tolerance response and formed significantly fewer biofilms ( P  &lt; 0.01). When analyzed by real‐time polymerase chain reaction, PdxR deficiency was found to drastically reduce expression of an apparent operon encoding a pyridoxal kinase ( SMU 865) and a pyridoxal permease ( SMU 866) of the salvage pathway of vitamin B 6 biosynthesis. In addition, PdxR deficiency also altered the expression of genes for ClpL protease, glucosyltransferase B and adhesin SpaP, which are known to play important roles in stress tolerance and biofilm formation. Consistently, PdxR‐deficiency affected the growth of the deficient mutant when grown in defined medium with and without vitamin B 6 . Further studies revealed that although S. mutans is known to require vitamin B 6 to grow in defined medium, B 6 vitamers, especially pyridoxal, were strongly inhibitory at millimolar concentrations, against S. mutans growth and biofilm formation. 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title Deficiency of PdxR in Streptococcus mutans affects vitamin B 6 metabolism, acid tolerance response and biofilm formation
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