Fig. 8. Neuronal differentiation requires Gcm activity in central brain. GFP immunolabeling in (A) control (gcm-gal4,tub-gal80^ts;UAS-ncGFP;UAS-gcm^N7-4DN) and (B) gcm-gcm2 loss-of-function (LOF) (gcm-gal4,tub-gal80^ts;UAS-ncGFP;UAS-gcm^DN) LIII CNS. Note that dcbcs and mcbcs (encircled by white and yellow dotted lines, respectively) are missing in gcm-gcm2 LOF but not in control animals as marked by the white and yellow asterisks in B. In these conditions of a single dose of the UAS-gcm^DN transgene, lamina development (neurons and glia) is less affected than with two doses of UAS-gcm^DN transgene (see Fig. S5 in the supplementary material). Arrows in A,B indicate processes of glia at the interhemispheric junction. (C,D) Development of central brain atonal-positive lineage is not affected by the gcm^DN construct. GFP immunolabeling in control (atonal-gal4,UAS-mCD8GFP in C) and gcm-gcm2 LOF (atonal-gal4,UAS-mCD8GFP,UAS-gcm^DN in D) LIII CNS shown in dorsal view. In control (C) as well as in gcm-gcm2 LOF (D) animals, atonal lineage includes two clusters of 20-30 neurons that are connected by a commissure crossing the midline (dashed line) and which extend a bundle of ipsilateral axons (arrows) into the optic lobes. Thus, gcm^DN expression does not affect the development of atonal-positive neurons. Scale bars: 100 µm in A,B; 180 µm in C,D.