Fig. 7: Menin inhibits the cross-talk between FGF2 and BMP2 by promoting Ptx3 expression in an H3K4me3 dependent manner.

a Genome browser view of normalized Menin and H3K4me3 ChIP-seq signals at Ptx3 promoter locus and RNA-seq tracks for Ptx3 in Men1^f/f and Men1^d/d decidual tissues. b Quantitative real-time PCR analysis of Ptx3 in Men1^f/f and Men1^d/d uteri on day 8. The values are normalized to Gapdh and indicated as the mean ± SEM (n = 3 biologically independent samples). Two-tailed unpaired Student’s t-test, ****p = 1.07e-5. c Quantitative ChIP analysis of Menin at Ptx3 promoter in uterine decidual tissue. Data represent the mean ± SEM. Two-tailed unpaired Student’s t-test, ***p = 0.0009. d Quantitative ChIP analysis of H3K4me3 at Ptx3 promoter in Men1^f/f and Men1^d/d uterine decidual tissue. Data represent the mean ± SEM (n = 3 biologically independent samples). Two-tailed unpaired Student’s t-test, **p = 0.0025. e In situ hybridization of Ptx3 in Men1^f/f and Men1^d/d uteri on day 8. Scale bar: 200 μm. f Immunoblotting analysis of the phosphorylation of ERK1/2 in mouse primary endometrial stromal cells treatment with FGF2 (20 ng/ml) in the absence or presence of PTX3 (100 ng/ml). Total ERK1/2 and β-Actin were used as loading controls. g Quantitative real-time PCR analysis of Ptx3 in primary mESC treated with DMSO or MI-503(2 μM) in vitro. The values are normalized to Gapdh and indicated as the mean ± SEM (n = 3 biologically independent samples). Two-tailed unpaired Student’s t-test, **p = 0.0053. h Immunoblotting analysis of Menin, BMP2, and phosphorylated ERK1/2 after the addition of PTX3 (100 ng/ml) or PD0325901 (5 μM) in mESC treatment with MI-503 (2 μM) in the presence of FGF2 (20 ng/ml). Total ERK1/2 and β-Actin were used as loading controls.