Fig. 4

Mutation in phr is causative for the regeneration defect in phr mutants. a–c Mauthner axon at 48 hpt distal and proximal to the transection site in stitched, low magnification images of a wild-type phr^+/+ axon (a), a heterozygous phr^tn207b/+ axon (b) and a compound heterozygous phr^tn207b/tp03 axon (c). Transection sites marked by a yellow arrowhead; rostrally directed projections in the phr^tn207b/tp03 compound heterozygote are marked by white arrows (C). Scale bar for a–c : 30 µm. Quantification of the extent of caudally directed regrowth in number of segments regrown caudally (d) and quantification of regrowth direction at the transection site (e), showing normal extent and directionality of regrowth in phr^+/+ and phr^tn207b/+ but reduced extent and misdirected regrowth in compound heterozygous phr^tn207b/tp03. This shows that the regeneration deficits observed in phr mutants are indeed caused by a mutation in phr. N = 48 phr^+/+, n = 53 heterozygous phr^tn207b/+ and n = 13 compound heterozygous phr^tn207b/tp03 were analyzed in (d, e). P-values were determined using two-tailed Student’s t-test (d), or Fisher exact test (e)