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. 2006 Apr 12;26(15):3999–4003. doi: 10.1523/JNEUROSCI.3845-05.2006

Figure 3.

Figure 3.

Overexpression of Sema1a induced the hyper-fasciculation of R-cell axons. A, Wild type (wt). B, Overexpression of Fas II in R-cell axons induced the formation of thicker bundles. C, Overexpression of Sema1a also caused a hyper-fasciculation phenotype. In larvae carrying two copies of the UAS-sema1a transgene (D), the phenotype becomes much more severe. R-cell axons form large clumps in the lamina and appeared to be unable to defasciculate and extend deeply into the medulla. In larvae carrying one copy of UAS-Fas II and UAS-sema1a (E), the phenotype is much stronger than that in larvae carrying a single copy of UAS-Fas II (B) or UAS-sema1a (C). The complete loss of the MICAL gene (F) did not suppress the Sema1a overexpression phenotype. Scale bar: (in A) 20 μm.