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. 2016 Sep 5;10:210. doi: 10.3389/fncel.2016.00210

FIGURE 3.

FIGURE 3

Sema-1a MB intrinsic and extrinsic effects. (A–D) OK107-Gal4-driven UAS-mCD8-Gfp labeling all MB lobes (green), Anti-FasII labeling α, β, and γ lobes (magenta). Confocal stacks (A) UAS-RNAi-Sema-1a; UAS-mCD8-Gfp; OK107-Gal4: MB lobes show outgrowth defects resulting in shorter α, β, γ, α′, and β′ lobes. (B,C) UAS-Sema-1a; UAS-mCD8-Gfp; OK107-Gal4. (B) α and β lobes show overextension (arrow). Most β axons show misorientation and project vertically besides the α lobe, resulting in a thin horizontal lobe (arrow head). α′β′ axons do not project properly and fuse (dashed arrow). (C) γ-lobes have abnormal morphology with tips growing up (arrow). (D) UAS-Sema-1aΔcyt2, UAS-mCD8-Gfp;OK107-Gal4: β and γ lobe show outgrowth defects resulting in shorter lobes. (E,E′,E′′) Frontal view of the pupal TIFR, 24 h after puparium formation. (E) Sema-1aCA07125: anti-GFP staining (green), Confocal stacks (E′) 442-Gal4/UAS-mCD8-Rfp: RFP expression in the TIFR (magenta). (E′′) Overlay. (F) Anti-FasII labeling α, β, and γ lobes. UAS-RNAi-Sema-1a; 442-Gal4: knock-down of Sema-1a in the TIFR results in β lobe overextension and fusion.