retn^z2-428/retn² flies eclose with only 8% of expected rates. retn^RU50/retn² flies eclose with only 58% of expected rates. Mutant females are strikingly resistant to male courtship. retn^RU50/retn² females copulate after an average 34+-6 minutes compared to an average of 3 minutes for wild-type. retn^z2-428/retn² females copulate after an average 58+-2 minutes compared to an average of 3 minutes for wild-type.

The early behaviour of the longitudinal glia appears normal in stage 11-14 retn¹/retn² embryos derived from homozygous female retn¹ clones. In stage 15-16 retn¹/retn² embryos, moderate but consistent fasciculation defects are seen in the longitudinal connectives. Some axons are not bundled correctly within the fascicles, which appear thinner and are occasionally found at the dorsal surface of the ventral nerve cord. The spacing between the first and second and between the second and third parallel bundles of the longitudinal connectives is slightly increased. In stage 16 retn¹/retn² embryos, the longitudinal glia occupy a normal position relative to the midline. However, the cells are shifted ventrally and are not localised to the characteristic flat cell sheet on the dorsal side of the longitudinal connectives (as occurs in wild-type embryos), with only one or two out of ten glial cells per hemineuromere being in any one focal plane. Some longitudinal glial cells in retn¹/retn² embryos are more rounded in shape compared to wild-type glia.

Homozygotes, hemizygotes and retn¹/retn² transheterozygotes die as embryos, but appear to have a normal cuticle pattern. retn¹/retn² embryos show loss of some groups of somatic muscles. Embryos both maternally and zygotically homozygous for retn² are produced by females carrying homozygous germline clones, but the efficiency of egg production is low. Many of the eggs are unfertilised and show early syncytial proliferation defects. These embryos can be partially rescued by a paternal retn⁺ allele; 16% of rescued embryos survive to the first instar larval stage. Embryos both maternally and zygotically homozygous for retn², but with a normal nuclear distribution show varying levels of disruption to segment formation, particularly in the posterior regions of the embryo. Most embryos also show abnormal germ-band retraction phenotypes that are not always rescued by a wild-type paternal retn allele. Head and tail defects are invariably seen, with one of the most consistent phenotypes being severe disruption of the cephalopharyngeal skeleton; the dorsal bridge, dorsal and ventral arms and mouth hooks are still recognisable, but the H-piece and lateralgraten are missing or severely malformed. Severe disorganisation of the somatic muscles including unfused myoblasts and non-specification and misdirection of muscle fibres is seen. The pharyngeal muscles have an atypical anterior position, indicative of disruption of head involution. All dorsally closing embryos lack pericardial cells.