pyr¹⁸/Df(2R)BSC25 mutant embryos exhibit random loss of cardioblasts (both generic cardioblasts and ostial cardioblasts), as compared to controls.

pyr¹⁸ embryos show a mild defect in the migration of ventral astrocytes, while the infiltration of astrocyte processes into the neuropil is not significantly different from that of controls.

pyr¹⁸ mutant embryos show a mild reduction in the number of longitudinal visceral muscle (LVM) fibres around the midgut, particularly in the anterior portion where LVM fibre spacing is wider and the first midgut constriction is either absent or reduced.

pyr^S0439/pyr¹⁸ mutant larval guts contain 5-8 longitudinal visceral muscle fibres per half side compared to 9-11 in wild type.

Adult homozygotes eclose at a rate of 0.71%.

Unequal spreading of mesoderm cells can be seen in stage 8 homozygous embryos. Subtle defects in mesoderm monolayer formation are seen.

Cells at the dorsal edge of the mesoderm form only short filopodial protrusions during dorsolateral migration in homozygous and pyr¹⁸/Df(2R)ED2238 embryos, in contrast to wild-type cells which form thin, long protrusions. The mutant cells fail to extend along the dorsal ventral axis.

Homozygous and pyr¹⁸/Df(2R)ED2238 embryos have disrupted dorsal vessel and dorsal somatic muscle development. In some cases, both cardioblasts and dorsal muscles are lacking in the same hemisegment, while in other cases a lack of cardioblasts does not correlate with a corresponding lack of dorsal muscles in the same hemisegment.

Homozygous and pyr¹⁸/Df(2R)ED2238 embryos have defects in the ventral oblique muscles VO4, VO5 and VO6. Duplications and loss of the segment border muscle are seen in homozygous embryos.