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Files in this Data Supplement:
Fig. S1. Nerve ring placement at L1 and L4 stages. The nerve ring was slightly more anterior in wild-type L1 animals than in L4 animals. In cam-1 animals, nerve ring positions shifted substantially between the L1 and L4 stage; this large-scale change was not observed in cwn-2 mutants, and correlated with CAN cell migration defects in affected animals (data not shown).
Fig. S2. Embryonic lethality induced by heat-shock expression of cwn-2 cDNA. Lethality was quantified as a reduced fraction of surviving L4 animals bearing the hs::cwn-2 transgene compared with control siblings. In non-heat-shocked animals, the array was transmitted to ∼60% of progeny.
Fig. S3. A cam-1(Δ417)::GFP transgene failed to rescue nerve ring defects in the cam-1(gm122) sax-3(ky200ts) sensitized background, but did rescue cam-1 or cam-1 mig-1 mutants. This transgene contained the extracellular and transmembrane domains of cam-1 fused to GFP. L4 sax-3 animals were scored at the permissive temperature of 15°C or the partially permissive temperature of 20°C. Asterisks, results different from controls at P<0.01 by t-test.
Fig. S4. Missing sublateral axons in cwn-2 mutants. (A-D) Electron micrographs of dorsal sublateral cords of wild-type animals (top, four axons per sublateral bundle) and cwn-2 animals (bottom, one or three axons per sublateral bundle).
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