Fig. 4: Osr1 deletion caused a migration problem of the SHF-derived Osr1+ cells.

A The R26R^fl/+;Osr1^GCE/+ embryos were given TM (75 mg/kg) at E7.5, E8.5, or E9.5, and β-galactosidase expression was evaluated in R26R^fl/+;Osr1^GCE/+ embryos at E14.5. Magnification = 50X. B Osr1-expressing cells migrated from the SHF into the atrial septum and pulmonary trunk between E9.5 to E13.5. TMX was given to the R26R^fl/+;Osr1^GCE/+ embryos at E8.5. The location of the SHF-derived Osr1+ cells, indicated by β-galactosidase expression, was evaluated at daily intervals from E9.5 to E13.5. C The tdTomato^fl/+; Osr1^LacZ/GCE embryos and the tdTomato^fl/+;Osr1^GCE/+ embryos were given TMX at E7.5 and E8.5, and the distribution of tdTomato+ cells was evaluated at E10.5. a, c: Grand view of the embryonic heart; b, d: Sections of OCT-embedded tissues. D a–d Osr1 deletion resulted in ectopic migration of the SHF-derived cells. The tdTomato^fl/+; Osr1^LacZ/GCE embryos and the tdTomato^fl/+;Osr1^GCE/+ embryos were given TMX at E7.5 and E8.5, and the location of tdTomato+ cells was evaluated at E12.5. a–d: Grand view of the embryonic heart. (e, f) LacZ staining was performed on Osr1^LacZ/GCE and Osr1^LacZ/+ embryos at E12.5. EOsr1 deletion inhibits cell migration, leading to reduced wound healing area. FOsr1 deletion inhibits the invasion of cells into the lower chamber. Data were expressed as mean ± SD. P values were defined as ***P < 0.001, *P < 0.05. LV left ventricle, RV right ventricle, LA left atrium, RA right atrium, ao aorta artery, pt pulmonary trunk.