Fig. 3: RUNX1 and FGFR2 modulate expression levels of SIX1 in MDE.
From: SIX1 cooperates with RUNX1 and SMAD4 in cell fate commitment of Müllerian duct epithelium
a SIX1 expression patterns in the vaginal fornices of Runx1 cHET and cKO mice at PD2 and PD4. In the fornix of Runx1 cKO mice, nuclear expression of SIX1 increases from PD2 to PD4, but the overall expression level of SIX1 in MDE remains low and uneven. b Violin plot of SIX1 IF signal distribution in the fornix of PD2 Runx1 cHET and cKO mice (n ≥ 4 per group). The signal distributions of two groups are significantly different (p < 2 × 10–16). c Expression of SIX1 in the vaginal fornix of Fgfr2 mutant mice. SIX1 is reduced in the fornix of Fgfr2 cKO mice, but the SIX1 expression level is restored by expression of MAP2K1DD. d Violin plot of SIX1 IF signal distribution in the fornix of PD2 Fgfr2 cHET, Fgfr2 cKO, and Fgfr2 cKO with MAP2K1DD (cKO + MK) mice (n = 4 per group). The signal distributions are significantly different among three groups (p < 2 × 10–16). e Regulation of SIX1 in cultured uterine explants. 20 ng/ml BMP4 has a weak effect on the expression of SIX1 in UtE. The combination of BMP4 (b), ActA (a), and FGF10 (f) (20 ng/ml each) induced nuclear expression of SIX1 and ΔNp63 in restricted regions of UtE. Replacement of FGF10 with Map2k1DD transgene (MK) efficiently induced SIX1 and ΔNp63 in UtE. f Violin plot of SIX1 IF signal distribution in the UtE of cultured uterine explants (n ≥ 4 per group). The signal distributions are significantly different among groups (p < 2 × 10–16). Bars = 100 µm.
