Neurl4^Δ1 mutants display a dominant misshapen primordial germ cells (PGC) in well over half of the embryos from heterozygous mothers. The frequency of PGC defects is similar in progeny embryos of Neurl4^Δ1/+ females crossed with either Neurl4^Δ1 or wild-type males, demonstrating that the PGC phenotype is independent of zygotic genotype. Embryos from wild-type females crossed to homozygous Neurl4^Δ1 males do not shot the PGC phenotype.

Embryos from Neurl4^Δ1 mutant mothers show multiple PGC defects at stage 10 during migration: the protrusion on PGCs are often smaller than normal; there are displaced vesicles just as seen in stage 5 embryos; and some PGCs are elongated relative to those in wild-type embryos.

Neither wild-type nor Neurl4^Δ1/+ mutant stage 5 embryos PGCs are positive for a marker of apoptosis.

Homozygous or hemizygous mutants are viable and appear healthy. However, a fraction of the progeny of Neurl4^Δ1 mutant mothers are agametic and thus infertile. Examination of embryos from Neurl4^Δ1 mutant mothers reveals that, in addition to the abnormal PGC morphology, the number of PGCs is reduced compared with wild-type.