lola^C28 mutants exhibit defects in embryonic germ cell migration. Although the mutant embryos show wild type early germ cell migration and the germ cells move into the mesoderm normally at stage 11, by stage 13 the germ cells do not align in a row and instead appear scattered. Similar, but slightly less severe, defects are seen in lola^C28/Df(2R)BSC595 transheterozygotes. Somatic gonadal precursor (SGP) specification and contact formation occur normally, but the fusion of the three SGP clusters that occurs in wild type does not always take place in lola^C28 mutant embryos, with one cluster (typically, but not necessarily the anterior) disjoined from the other two clusters. Unlike in wild type, many germ cells in stage 13 embryos are scattered in the vicinity of the gonad and are not always ensheathed by the SGPs. These mutant gonads fail to coalesce into the tight, round gonad seen in wild type. The SGP clusters that are occupied with germ cells remain elongated into the later stages of gonad development. lola^C28 mutant SGPs lack the actin-rich protrusions seen in controls. Fusion of other mesoderm-derived tissues appears unaffected: development of the visceral mesoderm is indistinguishable from wild type.

No gonad defects are observed in embryos containing lola^C28 mutant germline clones.

lola^C28/lola^22.05 mutant embryos exhibit gonad development defects that are similar in penetrance and severity to either lola^C28 or lola^22.05 homozygotes.

The longitudinal axon tracks in lola^C28 mutant ventral nerve cords appear wild type.