In Pvrc02195 mutant embryos, the anterior pair of Malpighian tubules fail to migrate into the anterior half of the embryo, instead they are observed projecting posteriorly.
The hemocytes of Pvrc02195 embryos fail to migrate in a wild-type pattern, and at stage 15 these hemocytes are observed clumped together in the anterior part of the embryo. At stage 17, the ventral nerve cord (VNC) is shorter in Pvrc02195 embryos than in wild-type, indicating that the VNC fails to condense correctly in Pvrc02195 mutants. This phenotype is fully penetrant.
Pvrc02195 homozygous clones have normal F-actin distribution, epithelial organization and polarity.
Border cell clusters in which all cells are homozygous for Pvrc02195 show delays in border cell migration, but the phenotype is incompletely penetrant and many border cell clusters complete their migration to the oocyte.
Mutants display a striking defect in hemocyte migration. Formation of hemocytes and their initial migrations are normal. By stage 11, posteriorly directed hemocytes reach the caudal margin normally. However unlike wild-type blood cells which rapidly enter the tail, blood cells in mutant embryos never enter the region, instead accumulating at the caudal margin. By stage 13 wild-type hemocytes are dispersed throughout the embryo, whereas mutant hemocytes are clumped together in aggregates concentrated in the anterior. No defects are detected in the CNS, muscles, and tracheal system, in mutant embryos.