Figure 4.

Kif1b loss of function does not affect Fignl1 enrichment in GCs. (A) In toto immunohistochemistry of Fignl1 in 26-hpf control and kif1bst43 mutant embryos focusing on SMN axons. The right-hand side of each genotype panel represents a higher magnification of the distal axon boxed in the corresponding left-hand panel. (B) Mean fluorescence intensity profile of Fignl1 along the distal portion of control (n = 35) and kif1bst43 (n = 78) mutant SMN axons. (C) Mean fluorescence intensity of Fignl1 staining in control (n = 41) and kif1bst43 (n = 50) spinal motor GCs with respect to the GC area. ns, nonsignificant (P > 0.05); unpaired two-tailed t test. Quantifications were performed in control (n = 9) and kif1bst43 (n = 13) embryos pooled from two independent experiments. Error bars are SEM. A.U., arbitrary units. (D) In toto immunohistochemistry of Fignl1 in 26-hpf control and kif1bst43 mutant embryos focusing on axons from the ventral longitudinal fasciculus. (A and D) Images are lateral views of the trunk, anterior to the left. Dashed lines delineate the GC surface. Scale bars, 10 µm.

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