Embryos have a pair rule phenotype. The segments that remain are about 1.4 times wider than wild-type segments and the cuticle is about 70% the length of a wild-type cuticle. The number of embryos that hatch and the number of adults eclosing is dramatically reduced compared to controls. ftz-dependent parasegments are enlarged and eve-dependent parasegments are reduced in stage 8 mutant embryos. The relative widths of enlarged and reduced parasegments remain relatively constant until germ-band retraction. Between stages 12-15 the relative widths of the smaller parasegments begin to decrease and by stage 16 reduced parasegments are no longer seen and the embryo is composed of seven enlarged parasegments. Parasegments 3 to 6 are unevenly spaced at stage 6-7 with parasegments 4 and 6 being about 1.4 times wider than wild-type and parasegments 3 and 5 being about 0.6 times the wild-type width. The wider parasegments contain about twice the number of cells of the narrower parasegments. The total width and number of cells in all four parasegments is equivalent to wild type. Each of the narrow parasegments maintains a constant relative width until around stage 12. After this time they decrease further in both width and cell number. The wide parasegments remain about 1.3-1.5 times wider and contain about 1.4 times as many cells as a normal parasegment. The pattern of cell death is abnormal in mutant embryos. Increased levels of apoptosis do not appear to be induced at or prior to stage 11 despite the earlier changes in parasegment size. By the end of stage 12 however, higher than normal levels of cell death are seen. The dying cells at this stage are almost exclusively in the wider parasegments, with few, if any, dying cells in the narrow parasegments. By stage 14, overall levels of apoptosis within the ectodermal layer have decreased. However, clusters of dying cells begin to appear below the surface of the narrow parasegments. These clusters increase in size and number at stage 15. At stage 12, cells of the narrow parasegments are seen to delaminate and move interiorly. The majority of these cells do not die until they have delaminated from the ectodermal layer, at stage 14, when the large clusters of dying cells begin to appear below the ectodermal surface.
Homozygous embryos have abnormally narrow odd-numbered parasegments at early stages of development which are eliminated at later stages.
eve1/eve5 larval brains show a significant reduction in normalised proliferation compared to controls.
Homozygous embryos show muscle abnormalities in abdominal segments 2 and 6. When mutant embryos are shifted to the restrictive temperature at 5 hours after egg laying most eve-expressing neurons form but the dorsal projections of motor axons are abnormal. The ISN is arrested prematurely in the ventral or dorsolateral region of the muscle field. By 9-10 hours AEL removal of eve function rarely affects ISN formation. Dorsal muscles form normally.
When eve1 embryos are shifted to the non-permissive temperature for 2 hours at early stage 11, the number of eve-expressing pericardial cells (EPCs) is reduced to on average only 24% of the wild-type number. Some of the EPCs that are present are located at some distance from the heart tube. DA1 muscle formation is also affected, but to a lesser degree. The reduction in the number of EPCs is less severe if the temperature shifts are earlier or later in development. The number of cardial cells, heart tube formation and overall body muscle formation are not significantly affected in eve1 embryos shifted to the restrictive temperature at early stage 11. Embryos shifted to the restrictive temperature at stage 11 show no morphologically detectable central nervous system defects. Temperature shifts at earlier stages perturb neural development (for example the RP2 neurons) and perturb visceral and somatic muscle formation.
Weak allele at 18oC, moderate allele at 29oC. At 18oC even-numbered denticle belts are variably deleted in homozygous embryos. At 29oC the frequency of deletions increases. At 31oC the ventral epidermis secretes a continuous lawn of denticles, which are derived from the 'fusion' of odd-numbered denticle belts. The phenotype of eve1 odd5 double homozygotes at 29oC is not an additive effect of the two mutations; the double mutant has 7 or 8 partial denticle belts, each with an apparent polarity reversal.
At the restrictive temperature of 31oC, homozygous embryos have a 'lawn of denticles' phenotype. At 25oC, homozygous embryos show a pair-rule phenotype. At 14 or 18oC, homozygous embryos show essentially normal segmentation.
Even numbered denticle bands missing.
Unsegmented lawn of denticle bands.