There is an increase in the number of synaptic boutons at the neuromuscular junction in mutant larvae.

The neuromuscular junctions of sgg¹⁰ larvae show an overgrowth phenotype. For example, there is an 80% increase in the number of type Ib boutons on muscle 6/7. sgg¹⁰/Df(1)64j4 larvae display a 60% increase in bouton number. There is also an increase in the number of "satellite" boutons, defined as boutons that are present in the axon of a branch or that bud off from neuronal connections between two boutons.

Hemizygous progeny derived from heterozygous females die during early larval stages. All embryos derived from homozygous germline clones die during embryonic development, and have very poorly differentiated cuticle which sometimes has holes in it. The head is defective, with abnormal spiracles, and the filzkorper material is very prominent. The CNS is very disorganised and the brain often protrudes dorsally rather than being covered by epidermis. The PNS is abnormal. Some embryos have a less extreme phenotype, with more cuticle differentiation and some defective denticle belt differentiation. The phenotype can be partially rescued by a paternal copy of wild-type sgg. Homozygous clones in the wing show homeotic transformation of hairs into bristles.

Homozygous germline clone cells were viable but produced eggs that exhibited morphogenesis arrest before cuticular differentiation. Mutant phenotype cannot be rescued by injection of wild type cytoplasm.

Growth rate slows during the third larval instar and they do not achieve full growth. Mosaic analysis demonstrates mutant phenotype is non-autonomous, clones survive as sectors of mutant tissue only in the abdomen.