All homozygous Mrtf^Δ7 mutant flies have a minor ventral indentation in the ellipsoid body neuropil. Visual orientation memory is slightly reduced, but is not significantly different from wild type. No defects are seen in heterozygotes.

Mutant flies have bristle defects. Homozygous follicle cell clones proliferate and differentiate normally. However, the basal network of actin filaments which is normally prominent in differentiated follicle epithelial cells is reduced in the mutant cells. Other F-actin structures are slightly reduced in mutant ovaries, such as cortical F-actin and ring canals in germline cells. Border cell migration is severely perturbed in the egg chambers of homozygous females; border cell clusters either do not initiate migration at all or migrate very poorly. Mutant border cells completely lack the enhanced F-actin accumulation that is normally seen in migrating wild-type border cells. Analysis of homozygous follicle cell clones indicates that the border cell migration defect is cell autonomous. At the stage when border cell migration normally begins, border cells in the egg chambers of homozygous females do produce long cellular extensions, as occurs in the wild type. However, subsequent to this, large round cytoplasmic fragments (without nuclei) appear to break off from the extension in the mutant cells. At later stages, the cell fragments are detected progressively further along the normal migratory path of the border cells. There is no evidence that these cytoplasmic fragments have any connection to the rest of the cell. The cytoplasmic fragments appear to move less efficiently than normal border cells, reaching the oocyte at a later stage than normal.

Hsap\MRTFB^{R104G.UAS.Tag:HA}, Mrtf^Δ7, Scer\GAL4^Mrtf-T2A.A has lethal phenotype

Mrtf[+]/Mrtf^Δ7, ebo⁶⁷⁸ has abnormal memory phenotype