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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.