Expression of mirr^Scer\UAS.cMa under the control of Scer\GAL4^nub.PU (restricted to 16 hours prior the third instar larval stage onwards using Scer\GAL80^ts.αTub84B) causes a significant reduction in the mitotic index in the wing disc.

Expression of mirr^Scer\UAS.cMa under the control of Scer\GAL4^Vm26Aa.F results in strong defects throughout the egg.

Expression of mirr^Scer\UAS.cMa in all SOPs, under the control of Scer\GAL4^scE1x6, causes a fate transformation of ventral cluster class II and III neurons, resulting in an increase in kn-positive neurons to 2 or 3, without changing the total number of neurons in the cluster. Ectopic mirr induces a class-IV-identity dendritic repulsion program in the terminal branches of the transformed neurons.

Expression of mirr^Scer\UAS.cMa in the v'ada lineage, under the control of Scer\GAL4^scE1x6, strongly induces midline crossing by the posterior branch of the v'ada axon terminal (84%). 62% of these altered axon termini exhibit additional small terminal ramifications projecting towards the midline.

Ectopic expression of mirr^Scer\UAS.cMa under the control of Scer\GAL4^{neur-GAL4-A101} results in a greatly heightened sensitivity to noxious stimulation, with larvae initiating a roll in 93% of trails. Only 56% of larval rolls are initiated in the expected anticlockwise direction, (compared to 79% in controls), suggesting that directional control over the escape response is lost.

Somatic clones of follicle cells in which mirr^Scer\UAS.cMa is ectopically expressed under the control of Scer\GAL4^Act5C.PI display apical constriction and nuclear organisation. In later stages, these cells are associated with ectopic appendage material. Although similar to the cell fate transformation resulting from loss of cic function is confined to the anterior half of the epithelium, the fate changes associated with mirr^Scer\UAS.cMa are observed even in posterior clones, suggesting that the competence to adopt this fate is restricted at the level of mirr regulation.

Misexpression of mirr^Scer\UAS.cMa, driven by Scer\GAL4^bi-omb-Gal4, in the ventral half of the eye allows the ectopic formation of dorsal rim ommatidia at the ventral extreme.

Somatic clones of mirr^Scer\UAS.cMa expressing tissue (driven by Scer\GAL4^Ubx.PdC) are abnormally large in medial parts of the tergite. The clones tend to be rounded and produce depigmentation. In addition most medial clones are associated with reversal of polarity of the hairs and bristles.

Overexpression of mirr^Scer\UAS.cMa under the control of Scer\GAL4^8.2 results in expansion of the dorsal appendages.

Expression of mirr^Scer\UAS.cMa under the control of Scer\GAL4^T155 results in enlargement of the dorsal appendages and in some cases multiple pseudo-dorsal appendages are formed. A loss of denticles is seen in 5-10% of the embryos derived from these eggs. Expression of mirr^Scer\UAS.cMa under the control of Scer\GAL4^C710 in females results in 95% of the eggs derived from these females having no chorion. Expression of mirr^Scer\UAS.cMa under the control of Scer\GAL4^E4 results in loss of posterior embryonic segments.

The size of the eye portion of the eye-antennal disc is reduced to about 2/3 of wild-type size in animals expressing mirr^Scer\UAS.cMa under the control of Scer\GAL4^ey.PH, and ommatidial differentiation is impaired.

Scer\GAL4^30A-mediated expression causes ommatidia near the ventral margin of the eye (near to area of mirr overexpression) to adopt dorsal polarity and chirality.