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. 2002 Jun 1;22(11):4448–4455. doi: 10.1523/JNEUROSCI.22-11-04448.2002

Fig. 5.

Fig. 5.

The netrin phenotype interacts weakly with slit. Fasciclin II labeling reveals defasciculation and gaps (arrow) in embryos homozygous for a small deficiency uncovering both netA andnetB (A, NP5/Y). Embryos heterozygous for the Netrin deficiency have similar but less severe irregularities in Fasciclin II distribution (B,NP5/+). Embryos lacking netrin function and heterozygous for slit reveal a netrinphenotype, with an increase in the frequency of midline guidance errors (C, NP5/Y; sli/+). Similarly, embryos doubly heterozygous for netrin and forslit (D, NP5/+; sli/+) or robo (E,NP5/+; robo/+) share the NP5/+ fasciclin II phenotype and a minor increase in the frequency of midline guidance errors (D, E, arrowheads). Midline guidance errors are not seen in netrin, scabdouble heterozygotes (F, NP5/+; scb/+).