Fig 2: Downregulated genes in Slc26a1-/- and Slc26a7-/- animals compared with wild types.The expression values of differentially expressed genes were normalized to those of Beta-Actin. For all the two-tailed t tests used, the significance level was 0.05. * <0.05; ** <0.01.

Fig 3: SEM images of mature enamel in Slc26a1-/- and Slc26a7-/- animals.The surface of the enamel of incisor and molars in Slc26a1 -/- and Slc26a7 -/- animals were similar to those of wild-type animals (A1-B3, magnification 35x). When the internal structures of enamel (incisor) were observed in coronal section (C1-C3, magnification 5000x), the enamel from mutant animals showed a mild disruption in rod density and diameter (C2-C3) compared with wild-type enamel (C1). The arrangement of the enamel rod and inter-rod structures (incisor) did not seem to be impacted significantly by the deletion of Slc26a1 or Slc26a7 (C1-C3).

Fig 4: Co-immunoprecipitation (Co-IP) assay of Cftr with Slc26a1, Slc26a6 and Slc26a7.Co-IP was conducted using protein samples extracted from the maturation-stage enamel organs of 4-week-old rat incisors (50~100 µg initial input). The interaction complexes were pulled down by anti-Cftr antibody (Table 3). The subsequent western blot analyses were performed using primary antibodies to Slc26a1, Slc26a6 and Slc26a7 (Table 3). The positive control was the pre-cleared total protein without the following immunoprecipitation procedures, and the negative control was prepared by skipping the step of applying the antibody against Cftr.

Fig 5: Real-time PCR analysis of Slc26a1, Slc26a6 and Slc26a7 expression during amelogenesis.The expression levels of Slc26a1, Slc26a6 and Slc26a7 were normalized to those of Beta-Actin and are presented in fold changes. The expression levels of Slc26a1, Slc26a6 and Slc26a7 were up-regulated by ~10.0, ~4.1 and ~15.3 fold, respectively, at maturation stage relative to secretory stage.