Fig. 8
From: Temporospatial inhibition of Erk signaling is required for lymphatic valve formation
Inhibition of Erk activity in FCLV contributes to valve-forming LEC specification. a In wild-type embryos, FCLV-LVs and FCLV-PHS LVVs can be formed appropriately to ensure the unidirectional flow of lymphatic fluid and prevent the backflow of blood into the lymphatic circulation. b In the embryos with Efnb2-Ephb4-Rasa1 cassette mutations, FCLV-LVs and FCLV-PHS LVVs are defective, therefore leading to a kind of lymphatic blood-filling phenotype. c Vegfc-Vegfr3-mediated Erk activation in luminal LECs of the aLFL. d Efnb2-Ephb4-Rasa1 works in Erk inhibition to induce extremely high Prox1 expression in valve-forming cell specification. PHS primary head sinus, FCLV facial collecting lymphatic vessel, aLFL anterior part of lateral facial lymphatic vessel, pLFL posterior part of lateral facial lymphatic vessel, LV lymphatic valve, LVV lymphovenous valve. Venous endothelial cells (blue), the aLFL LECs with activated Erk signaling (orange), the FCLV LECs with repressed Erk signaling (green), Efnb2-expressing LECs (cyan), lymphatic valve to be formed (cyan with dashed lines), and FCLV-PHS LVV (purple) are indicated. The figure was created using Adobe Illustrator 2021
