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. 2006 Jul;173(3):1241–1258. doi: 10.1534/genetics.106.057000

TABLE 3.

Ray 1 axon defects

Ray axon morphology
graphic file with name GEN17331241inf3a.jpg graphic file with name GEN17331241inf3b.jpg graphic file with name GEN17331241inf3c.jpg graphic file with name GEN17331241inf3d.jpg graphic file with name GEN17331241inf3e.jpg graphic file with name GEN17331241inf3f.jpg graphic file with name GEN17331241inf3g.jpg
Genotype Wild type (%) Wandering (%) Ectopic outgrowth (%) No ventral turning (%) Anteriorly ventral turn (%) Bifurcating (%) Cell migration (%) N
him-5(e1490) 97 2 0.4 228
rax-1(bx126) 51 11 26 3.3 8.5 274
rax-1(bx132) 20 16 49 3.9 8.1 405
rax-4(bx139) 39 2 48 5 6 288
rax-2(bx131) 82 16 2 100a 84
rax-3(bx133) 73 27b 78 101
rax-3(bx138) 81 19b 77 170
rax-5(bx137) 70 7 13 10 17c 225
rax-6(bx140) 77 7 16 48c 109
bx141 73 27 68
sax-2(bx130) 100 200
unc-27(bx124) 9 79 12 153

The percentage of sides with ray 1 defect is shown. Defects in the ray 1 process were the most easily scored and most likely to be abnormal. With the exception of rax-1 and rax-4, ray commissures of the posterior rays were usually present in mutants.

a

80% of males have more than 8 pkd-2∷GFP positive neurons in the tail, in addition to the anterior mispositioned ray neuons.

b

Ray axons from 27% and 19%of sides in bx133 and bx138 mutant, respectively, fail to make the ventral turn when the neurons are mispositioned anteriorly. The rest of the neurons extend posteriorly-directed axons.

c

The neurons of fused rays form cluster in the lumbar ganglion. Axon defects and cell migration defect are counted separately.