Mutants show a delay in thoracic neuroblast 3-3 (NB3-3T) entering quiescence, and a corresponding increase in the number of EL neurons. Despite the delay, NB3-3T eventually enters quiescence as no proliferating NBs are found in the thorax of newly hatched sqz⁰²¹⁰² larvae.

Marker analysis indicates that Tv neurons are absent from sqz⁰²¹⁰² homozygous first instar larvae. sqz⁰²¹⁰² somatic clones do not cause any visible phenotype in adult wings.

The sqz⁰²¹⁰²/Df(3R)Dl-KX23 combination show considerable lethality during pupal stages. Mutant larvae are lethargic, display an apparent loss of balance whereby larvae are often observed laying in their side and demonstrate a motility defect whereby the body wall musculature overcontracts during the peristaltic wave typical of insect larval motility. The motility phenotype is fully penetrant. Those animals that eventually eclose are grossly normal although a failure of wing inflation and proboscis defects are seen. However the eclosing adults are entirely immotile except for a persistent tremor. These adults die within 24 hours.

sqz⁰²¹⁰²/Df(3R)Dl-KX23 mutant larvae display a motility defect whereby the body wall musculature over-contracts radially during the peristaltic wave typical of larval motility, apparent as a 'squeezing' of the intestine. This phenotype is fully penetrant. In mutants a frequent failure (~1/3) of the Tv axon fails to innervate the dorsal neurohemal organs.

Homozygotes die during the first and second larval instar stages. Females carrying homozygous germ line clones lay few eggs, which have defective dorsal appendages.

Germline clones produce abnormal eggs due to abnormal oogenesis: few eggs are laid that exhibit defective dorsal appendages.