Six4¹⁰⁸ homozygotes and Six4¹⁰⁸/Six4²⁸⁹ transheterozygotes are lethal.

Homozygous follicle cell clones can induce neighbouring anterior follicle cells to form ectopic, migratory border cell clusters.

Embryos homozygous for Six4²⁸⁹ exhibit very few srp-positive cells in the trunk at stage 14, as oppose to wild-type embryos, in which these cells form a continuous layer in the lateral mesoderm. There appears a defect in initial specification of the primary fat body precursors in stage 10-12 mutant embryos.

Many of the somatic gonadal precursors that initially appear in Six4²⁸⁹ mutants appear to die subsequently. The number of cells expressing eya decreases markedly during stage 12, while a greater number of apoptotic cells is observed in the region normally occupied by somatic gonadal precursors.

Six4²⁸⁹ mutants exhibit a characteristic pattern of muscle defects. The cardioblasts appear normal, as do the dorsal somatic muscles while lateral and ventral somatic muscles are severely disrupted. The lateral body wall muscles are severely affected, with many muscles absent. In the ventral region, the ventral acute muscle, VA3, and segment border muscle, are absent in most segments, while some ventral oblique muscles and most of the ventral longitudinal muscles are usually present.

Homozygotes fail to hatch. Embryos have gonadal coalescence defects. The embryonic muscle pattern is disrupted. Muscles appear disorganised in their arrangement and attachment. Some muscles appear to be entirely missing, although the number and location of such muscles varies between segments and embryos. The primary defect appears to be in the fusion process.