Skip to main content
. 2009 Feb 11;136(6):943–953. doi: 10.1242/dev.029363

Table 2.

Quantification of process defects in mig-32 mutants

Genotype Cell process Animals with a defect (%) n
Pnlp-1gfp HSN axon 0 50
mig-32(n4275), Pnlp-1gfp HSN axon 56 49
mig-32(tm1684), Pnlp-1gfp HSN axon 46 46
mig-32(tm1807), Pnlp-1gfp HSN axon 56 88
Psra-6gfp PVQ axons 8 50
mig-32; Psra-6gfp PVQ axons 26 87
Punc-47gfp VD commissures 4 25
mig-32; Punc-47gfp VD commissures 63 100

The percentage of animals with a defect in specific neuronal processes is shown. For the HSN axons, animals were scored as defective if the axon failed to reach the head; in general, axons that reached the head followed a normal path from the HSN ventrally into the ventral nerve cord then turned anterior to the head. HSN neurons that failed to migrate to the midbody often had more severe defects in axon pathfinding, with axons that tracked posterior rather than anterior. For the PVQ axons, defective axons included those that crossed the midline inappropriately, as compared with wild-type animals. For the VD commissures, defective commissures included those that tracked on the wrong side of the body wall. mig-32 mutants had 0-5 commissures on the wrong side, with posterior VD neurons being more likely to have defective commissures