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. Author manuscript; available in PMC: 2019 Feb 1.
Published in final edited form as: Environ Microbiol Rep. 2017 Dec 4;10(1):12–22. doi: 10.1111/1758-2229.12600

Table 3.

S. mutans clinical isolates contain polymorphisms within oxidative stress genes when compared to UA159

Gene Enzyme Function Polymorphisms*
ahpF Nox-1 NADH oxidase Reduces 2NADH + O2 -> H2O2 Smu81 A195 to T; P197 to S
ahpC Alkyl hydroperoxide reductase Deactivates H2O2 100 % identical
dpr Dps-like peroxide resistance gene Fe+ binding protein - prevents Fenton reactions Smu81 T43 to A
nox-2 NADH oxidase H20 forming NADH oxidase Smu81 R130 to C; H324 to Y; T459 to I
Smu56 D233 to N; R430 to H
Smu44 T430 to I
spxA1 Transcriptional regulator Major regulator of oxidative stress genes Smu81 A18 to T; S35 to N; K99 to R

Polymorphisms are based on sequence alignments performed using shotgun genome sequence for clinical isolates compared to S. mutans reference strain UA159. NCBI accession numbers for each strain are listed in Table 1. Note: The gene for superoxide dismutase (Smu.620) was 100% identical in all strains.