Fig. 9. RA-Tgfß-Fgf10 interactions during primary lung bud formation in the mouse. (A) In an RA-sufficient foregut, endogenous RA maintains low levels of Tgfß signaling in the mesoderm of the lung field to allow Fgf10 expression and lung bud initiation. (B) Under conditions of RA-deficiency, Tgfß signaling is abnormally hyperactivated, thereby blocking Fgf10 expression and lung bud formation.