The bipotential Ganglion Mother Cells, or GMCs, in the Drosophila CNS 
asymmetrically divide to generate two distinct post-mitotic neurons. Here, we 
show that the midline repellent Slit (Sli), via its receptor Roundabout (Robo), 
promotes the terminal asymmetric division of GMCs. In GMC-1 of the RP2/sib 
lineage, Slit promotes asymmetric division by down regulating two POU proteins, 
Nubbin and Mitimere. The down regulation of these proteins allows the asymmetric 
localization of Inscuteable, leading to the asymmetric division of GMC-1. 
Consistent with this, over-expression of these POU genes in a late GMC-1 causes 
mis-localization of Insc and symmetric division of GMC-1 to generate two RP2s. 
Similarly, increasing the dosage of the two POU genes in sli mutant background 
enhances the penetrance of the RP2 lineage defects whereas reducing the dosage 
of the two genes reduces the penetrance of the phenotype. These results tie a 
cell-non-autonomous signaling pathway to the asymmetric division of precursor 
cells during neurogenesis.