Mutants are female sterile, embryonic lethal and produce membrane growth defects in cellularization. Adults show variable wing and leg defects.

dop¹ mutant embryos exhibit delayed growth of malformed furrows during cellularization. Furrow widths are unimpaired during syncitial development, but during cellularization they are significantly wider and irregular compared to controls.

Initiation of furrow formation is blocked in dop¹ mutant embryos - furrow canals are absent during the first 20 min after the onset of cycle 14.

In early cellularization, there is no detectable difference in the distribution and size of the villous projections at the cell surface; however, towards the end of cellularization, long projections persist in dop¹ mutants whereas the surface becomes smooth in wild type.

A low percentage of dop¹ flies exhibit partial deletion of wing margins, particularly at the posterior, and defective wing venation.

Embryos derived from homozygous females show a severe delay in membrane ingression during cellularisation and have an abnormal lipid-droplet distribution during germ-band extension.

Flies homozygous or hemizygous for dop¹ are viable, but embryos from dop¹ mothers do not hatch and display defects in larval cuticle formation. There are no significant differences between wild-type and dop¹ mutant embryos up to cycle 13. However, events at the midblastula transition are affected in the mutant embryos. For example, the formation and growth of cell membranes at the start of and during cellularization is defective. dop¹ embryos are abnormally transparent from gastrulation onward with lipid droplets highly enriched basally around the yolk sac, instead of being present throughout the embryo periphery. Wild-type and dop¹ embryos display similar levels of transparency up until the end of cycle 14 and initial basal droplet transport is normal in the mutants. Therefore, a developmentally regulated switch in organelle transport appears to be defective in dop¹ embryos at the end of cellularization.

Developmental defects occur during the transition from the syncytial to cellular blastoderm, causing abnormal cellularization. The distinct separation of the yolk and cortical cytoplasm breaks down followed by the irregular distribution of somatic nuclei.

Embryos derived from homozygous females show defects in cellular blastoderm formation. Cycle 14 embryos contain multiple nuclei that have been displaced from the peripheral monolayer and show irregularities in the cortical cytoplasm. The membrane furrows invaginate to different levels, and the greatest depth of the furrows is substantially less than that seen in wild-type embryos. Despite the absence of a uniform monolayer of nuclei at the embryo surface, the cortical actin network does form, with only one nucleus present per cell. The nuclei of the mutant embryos fail to elongate normally.

The initial cytoplasmic clearing and distinct separation of the peripheral cytoplasm from the central yolk appears to occur normally in embryos derived from dop¹/Df(3L)BK10 females during syncytial blastoderm formation. However, the normal uniform appearance of the cytoplasm is not maintained in the mutant embryos, and irregularities are seen soon after the nuclei enter cycle 14. With time, the yolk/cortical delimitation becomes more irregular and many nuclei become displaced from the peripheral monolayer.

Embryos derived from mutant females show variable cuticle differentiation, with defects ranging from a slightly deformed cuticle with normal abdominal denticle belts but showing head defects to severe abnormalities with missing abdominal cuticle and head defects.

dop¹ has wing margin phenotype, enhanceable by sw¹/sw¹

dop¹ has wing vein phenotype, enhanceable by sw¹/sw¹

dop¹ has membrane | embryonic stage 5 phenotype, enhanceable by sw¹

dop¹ has membrane | embryonic stage 5 phenotype, enhanceable by DCTN1-p150^Gl-1

dop[+]/dop¹ is an enhancer of eye phenotype of DCTN1-p150^Gl-1

dop[+]/dop¹ is an enhancer of wing margin phenotype of sw¹

dop¹/dop¹ is an enhancer of wing margin phenotype of sw¹

dop¹/dop¹ is an enhancer of wing vein phenotype of sw¹