Figure 7.

eFGF2 acts via MEK to maintain progenitor identity

(A) Experimental diagram of mechanism experiments. Cortical progenitors were exposed to eFGF2 (±MEKi) to analyze the role of MEK.

(B) eFGF2-treated cultures did not generate TBR2⁺ IPCs, an effect that was reversed by MEKi.

(C) Likewise, eFGF2 cultures generated limited TBR1⁺ neurons at D26, in contrast to Basal conditions. This effect was also reversed by MEKi.

(D–H) Quantification at D26 for TBR2 (D), TUJ1 (E), TBR1 (F), CTIP2 (G), and BRN2 (H) under Basal, eFGF2 and eFGF2⁺ MEKi conditions (n = 3 independent experiments).

(I) Putative role of FGF2 signaling during cortical maturation and laminar specification.

Scale bar, 50 μm.