Fig 1: Palatal phenotypes of K14-Cre/Runx1fl/fl mice. (A–C) Immunostaining for K14 at the boundary between the primary and secondary palate. (A) In controls, the epithelial remnants (arrowheads) are formed in the process of anterior palatal fusion. (B) In Runx mutants, 75% had partial contact at E15.0, and K14-immunoreactive epithelial remnants (B, arrowhead) were retained between the primary and the secondary palate: (C) 25% of the mutants did not have any contact. Scale bar: 100 µm. (D–G) TUNEL staining of frontal sections of the primary and secondary palates at E15.0. Scale bar: 100 µm. TUNEL-positive cells were fewer and sparse on the unfused epithelium in Runx1 mutants. (H) The percentage of TUNEL-positive cells on the contacting epithelium. (I,J) Immunostaining for Ki67(green) and K14(red) revealed less proliferative cells in the epithelial remnants in wild-type mice (I), while some Ki67 signals were retained in the epithelial remnants in Runx1 mutants (arrowheads in J). Scale bar: 50 µm. (K) The percentage of Ki67 positive cells. (L,M) Immunostaining for K17 (green) revealed that K17-immunoreactive periderm cells were retained on the surface of the nasal septum and the nasal side of the secondary palate in Runx1 mutants. Nuclei were counterstained with DAPI (blue). The arrowhead indicates persistent periderm (arrowheads in M). Scale bar: 100 µm. (N,O) BrdU staining revealed that there were no marked changes in the BrdU signals in the palatal mesenchyme due to Runx1 deficiency at E15.0. Scale bar: 200 µm. pp, primary palate; sp, secondary palate; ns, nasal septum; vo, vomeronasal organ.