Expression of mys^GD15002 under the control of Scer\GAL4^hth-GETDB in larval antennal discs does not lead to any obvious defects in the formation of the A1 fold or segregation of cells with respect to the field boundary at the A1 fold, but mutant cells exhibit some morphological defects, such as swelling, enlargement, or delamination, as compared to controls.

Scer\GAL4^nSyb.PS-driven, presynaptic expression of mys^GD15002 blocks activity-induced (upon high K[+] stimulation) enlargement of neuromuscular junction boutons in third instar larvae whereas Scer\GAL4^how-24B-controlled (combined with tub-Gal80[ts] to limit the expression to larval stage and avoid lethality), postsynaptic expression does not.

Expressing mys^GD15002 under the control of Scer\GAL4^repo (in combination with a Dicer-2 transgene to enhance RNAi efficiency) results in decreased glial cell numbers in the eye discs of second and third instar larvae. Photoreceptor axon targeting to the optic stalk is unaffected.

Expression of mys^GD15002 RNAi under the control of Scer\GAL4^pnr-MD237 (but not Scer\GAL4^A58) results in large syncitia being formed both at boundaries and intrasegmentally (reflecting the gradual spatial restriction of the driver expression pattern) in third instar larval epidermis and also leads to detachment of muscle fibers from tendon cells.

Expression of mys^GD15002 under the control of Scer\GAL4^Hand.PA results in a severe defect in the adult heart muscle, with the cardiomyocytes showing a 'rounded-up' phenotype.

Expression of mys^GD15002 under the control of Scer\GAL4^NP5130, in combination with a Gal80[ts] transgene to restrict expression to the two weeks of adulthood prior to analysis, results in a reduction in Esg-positive progenitors, including a reduction in intestinal stem cell numbers, in the adult posterior midgut, with with a decrease in cell division (PH3 staining) and no increase in apoptosis (TUNEL assay).

When mys^GD15002 is expressed in third instar larvae under the control of Scer\GAL4^21-7 (and co-expressed with Dcr-2^Scer\UAS.cDa) 24.33% of the length of the ddaC dendrites at the dorsal midline are enclosed in the epidermis rather than attached to the ECM compared to only 5.69% in controls.

Adults expressing mys^GD15002 under the control of Scer\GAL4^elav.PLu (in the presence of Dcr-2^Scer\UAS.cDa to increase the efficiency of RNAi) do not show a significant defect in avoidance of noxious temperature (46[o]C) compared to control flies.

Depending on the insertion line used, expression under the control of Scer\GAL4^Mef2.PR can result in embryonic lethality or late larval lethality.

Expression under the control of Scer\GAL4^Mef2.PR results in rounded larval body wall muscles.

Expression under the control of Scer\GAL4^Mef2.PR results in sarcomere defects in the larval body wall muscles.

Expression under the control of Scer\GAL4^pnr-MD237 results in lethality (either before or at the pupal stage), depending on the insertion line used.

Hub cells often fail to localise to the apical tip of the testis in males expressing mys^GD15002 under the control of Scer\GAL4^C587.

Scer\GAL4^NP5130, mys^GD15002 has decreased cell number | adult stage phenotype, non-suppressible by Ras85D^V12.UAS, Scer\GAL4^NP5130

Scer\GAL4^NP5130, mys^GD15002 has decreased cell number | adult stage phenotype, non-suppressible by BacA\p35^UAS.cHa, Scer\GAL4^NP5130

Scer\GAL4^NP5130, mys^GD15002 has adult posterior midgut epithelium phenotype, non-suppressible by Ras85D^V12.UAS, Scer\GAL4^NP5130

Scer\GAL4^NP5130, mys^GD15002 has adult posterior midgut epithelium phenotype, non-suppressible by BacA\p35^UAS.cHa, Scer\GAL4^NP5130