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DOI: http://dx.doi.org/10.7554/eLife.03962.006 Since we observed dramatic Purkinje cell migration defects, we next examined the status of radial glial cells and Bergmann glia.

To assess whether loss of DG in PC is adequate to cause migration defects, we evaluated the histopathology of PCP2-Cre/DG-null mice.

Because hse-5 caused AQR and PQR migration defects, we wanted to analyze the effect of other C. elegans HSPGs in AQR and PQR migrations.

The migration defects we observed in tissue expressing N-APC fragments raised the possibility that N-APC fragments have an effect on cell behaviour that is dominant over the remaining wild-type APC allele.

To further characterize Pak-dependent DTC migration defects, we built pair-wise double mutant strains with mutations in pak-1 (ok448 and tm403 ) and max-2 (nv162 and cy2 ).

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This allowed us to determine whether the migration defect we observed in APC Min/+ tissue was a direct effect of an N-APC protein fragment.

If the fecundity defect in mir-83 (n4638 ); mir-34 (gk437 ) hermaphrodites was a direct consequence of the gonad migration defect, we would expect to see a greater number of cross-progeny produced by mir-83 (n4638 ); mir-34 (gk437 ) mutants when raised at 20° compared to temperature cycled, as temperature cycling dramatically decreases the percentage of animals with normal gonad morphology.

These findings are consistent with the migration and localization defects we observed in competitive contexts, and they indicate that comp-1 defects are not solely induced by the presence of wild-type sperm.

In P7 SynIII shRNA-transfected brains, we found migration defects and significant cell misorientation similar to that observed in superficial layers.

In a previous genome-wide RNA interference (RNAi) screen for animals with DTC migration defects (Cram et al. 2006) we identified CACN-1 as a well-conserved and novel regulator of cell migration.

We confirmed the migration defects in progeny pgc mutant mothers.

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