Figure 8
Proposed model for ephrin-A2’s role. In normal wildtype, activation of ephrin-A2 reverse signalling following interaction with Eph promotes the asymmetrical or terminal symmetrical division of apical progenitors in the VZ to generate neurons through activation of a pro-neural pathway. In knockout animals, in absence of pro-neural signals, apical progenitors undergo symmetrical self-renewing division leading to a deficit of glutamatergic neurons in the developing cortical plate and accumulation of progenitors. These missing neurons are apparently replaced by other cells which identity is yet to be determined.
