Homozygous clones in the adult thorax result in a loss of hairs and a gain of socket cells.

In seq²² mutant homozygous clones, a large proportion of R7 cells terminate their axon projections in the outer M1-M3 layers, rather than the M6 layer. seq²² mutant R8 axons frequently stop above their prospective M3 target layer. When homozygous seq²² mutant clones are induced specifically in the R7 cells, almost all of the R7 axons stop prematurely in M3, even when surrounded by heterozygous R8 and R7 axons.

Single cell class IV dendrite arborisation (da) neuron clones that are homozygous for seq²² do not show defects in the establishment or maintenance of dendritic tiling.

Dendritic field formation by mutant type IV da neurons appears normal.

The embryonic peripheral nervous system (PNS) of seq²² homozygotes has increased numbers of multidendritic (md) neurons, and decreased numbers of external sensory neurons. The md neurons in these mutants exhibit excessive, dorsally oriented dendrite outgrowth. The resulting dendrites are abnormally long at late embryonic stages and cross the dorsal midline, a behaviour that their wild-type equivalents are too short to achieve. Time lapse analysis reveals that these dendrites do not extend faster than in wild-type. Instead their growth is initiated earlier, and carries on later than in wild-type embryos: at 11-12 hours after egg laying (AEL) 85% of seq²² homozygotes show significant mdc dendrite growth, compared to only 10% of wild-type embryos of this stage; at 16-17 hours AEL, when the md dendrites in wild-type embryos stop extending dorsally, dorsal extension of mutant md dendrites continues. Unlike in wild-type, seq²² homozygotes at 11-12 hours AEL lack the morphologically distinct dendrites produced by external sensory (es) neurons. Some multidendritic neurons in mutants are located more dorsally than in wild-type, at locations normally occupied by es neurons. This latter group tend to fasciculate their dendritic processes together, and extend fewer lateral branches. In seq²² homozygotes all classes of embryonic peripheral nervous system (PNS) neurons have prematurely terminating axons, resulting in complete axon breaks between PNS clusters. Fewer axons emerge from the dorsal clusters of neurons in the embryonic peripheral nervous system, and those that do are frequently misrouted or prematurely stopped in their path towards the central nervous system (CNS). The CNS of these embryos shows a similar axonal phenotype to the PNS: Large fascicles of longitudinal axon tracts evident in the CNS of wild-type embryos are absent in mutant embryos. In addition, motor neuron projections to the periphery are greatly reduced. External sensory neurons associated with seq²² somatic clones in the notum and scutellum have a range of morphological defects: some neurons have thick dendrites and laterally protruding processes, while other neurons fail to extend dendrites to innervate the accompanying hair. Macrochaete and microchaete encompassed by these clones form normally. In eyes with composed exclusively of seq²² somatic clone cells, ommatidial morphology is normal but axonal projections of the photoreceptors are defective: the regular array of axon bundles seen in the lamina and medulla of wild-type eyes is either malformed or completely absent. (Note: somatic clones generated in a background with W^GMR.PG on the homologous arm to that carrying seq²², so that only seq²² homozygous cells (which lack W^GMR.PG) survive in the eye.)

Exhibits excessive dorsal branch outgrowth in the dorsal cluster of embryonic dendrites. Dorsal branches in most hemisegments fail to stop at the appropriate time, and instead continue to extend toward the dorsal midline, eventually crossing the midline and mixing with dendrites of the dorsal cluster in the other hemisegment by stage 17. This phenotype is highly penetrant. The dendrites of the md neurons of the lateral cluster also extend abnormally long distances. Mutant embryos also exhibit axonal outgrowth defects; the axons from dorsal cluster neurons or from chordotonal neurons fail to extend towards the central nervous system (CNS). Axonal breaks are also seen in the CNS. Mutants show no gross defects in anterior-posterior or dorsal-ventral patterning.