Mis-expression of lbe^Scer\UAS.cJa under the control of Scer\GAL4^kirre.PR results in the formation of DA1, DT1 and VA2 having seven nuclei which is lower than that in wild-type.

Ectopic expression of lbe^Scer\UAS.cJa under the control of Scer\GAL4^kirre.PR is sufficient to change the DA1 embryonic myoblast fusion rate to SBM-like one.

Myoblast driven expression of lbe^Scer\UAS.cJa (under the control of Scer\GAL4¹¹⁵¹) leads to severe defects in the patterning of dorsally located leg muscles. The tibia talm muscle is abnormally shaped and the homologous levator muscle in the femur is completely disrupted. A large proportion of dorsally located femur fibres normally contributing to the tilm muscle are unable to attach to the tilt tendon, most probably leading to its degeneration. Instead, they attach on both sides to the disc epithelium, adopting orientations perpendicular to the proximal-distal axis. In addition, some ectopic dorsal muscle fibres are observed in the proximal part of the tibia and femur.

Expression of lbe^Scer\UAS.cJa under the control of Scer\GAL4¹¹⁵¹ results in poor locomotor co-ordination and a spread-out positioning of the legs with respect to the body axis. The ability of these flies to catch, maintain and rotate a polystyrene ball are also impaired. About 60% of flies are unable to catch the ball and more than 80% lose it in less than 30 seconds, whereas wild-type flies do not have a problem with this.

When lbe^Scer\UAS.cJa is driven by Scer\GAL4^{l(3)31-1-31-1} defects in CNS morphology is seen. There is a thinning or absence of the posterior commissures in some neuromeres and a fusion of the commissures in others. The EL neurons deriving from NB 3-3 are also defective. Supernumerary subperineural and exit glial cells are also seen. The distance between the ISN and SN nerve clusters is decreased.

In lbe^Scer\UAS.cJa; Scer\GAL4^tin.cBa, there are no obvious gain-of-function induced alterations in the patterning of the cardiac outflow region. In contrast, lbe^Scer\UAS.cJa; Scer\GAL4^how-24B embryos exhibit abnormal contact of the cardiac outflow muscles with the tip of the heart. Most precisely, the cardiac outflow muscles attach directly to the most anterior cardiac cells that form the cardiac outflow and not to the second pair of cardiac cells as in the wild-type. In addition ventral bending of the most anterior part of the heart is more pronounced than in wild-type, and the cardiac outflow muscles themselves. However, the contact between heart anchoring cells and cardiac cells is not affected.

When lbe^Scer\UAS.cJa is driven by Scer\GAL4^how-24B leads to a 60% loss in muscle DA1 founders and a 40% loss of DO1 founders.

Embryos expressing lbe^Scer\UAS.cJa under the control of Scer\GAL4^how-24B have enlarged or duplicated segmental border muscles (SBMs) in approximately 70% of hemisegments. The number of lateral adult muscle precursors (LaPs) is significantly increased. The overproduction of SBM and LaPs is frequently associated with the loss of some neighbouring lateral muscle fibres. The number of ventral adult muscle precursors is significantly reduced.