Expression of rhea^GD12050 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.

Expression of rhea^GD12050 driven by Scer\GAL4^Hand.PU throughout larval stages results in pupal death; hearts in adult escapers have a collapsed myofibril network, with actin bundles surrounding each myocyte nucleus. Continuous depletion (rhea^GD12050 driven by Scer\GAL4^Hand.PU) leads to hearts and aortas with an increased diameter in the third instar larva, compared to wild type; some cardiomyocyte processes lack myofibril or sarcomere structure and some retract into thick cells, exposing naked extracellular matrix. Expression of rhea^GD12050 driven by Scer\GAL4^Hand.PU during the first instar stage (controlled by Scer\GAL80^ts.αTub84B) leads to hearts in third instar larvae that are not capable of complete contraction.

First instar larvae with expression rhea^GD12050 driven by Scer\GAL4^Hand.PU (with Scer\GAL80^ts.αTub84B) have irregularly placed cardiomyocytes that are largely detached from each other and dilated hearts compared to controls. Depletion during the second instar stage results in minor cardiomyocyte defects, lacking uniform midline apposition and myofibrils of adjacent myocytes do not connect or align at myocyte junctions. Depletion during metamorphosis results in greater myofibril retraction (but not heart dilation). Depletion during adulthood slightly widens midline apposition of cardiomyocytes. Depletion at any larval stage significantly reduces heart contractility (most severely during the first instar stage); heart rhythmicity is reduced if depletion occurs during the first or both the second and third instar; dilation is increased only with depletion during the first instar stage; there are no significant effects on heart rate.

Expression of rhea^GD12050 driven by Scer\GAL4^Hand.PU (with Scer\GAL80^ts.αTub84B) during the first instar stage leads to mostly pupal death, with some short-lived escapers; depletion during second or second and third instar stages leads to more escapers that are somewhat short-lived (expression during L2 leads to 50% lethality at 81 days versus 132 days in controls); depletion during third instar (L3) or pupal and adult stages (PA) leads to short-lived flies (50% lethality for L3 at 4 days versus 37 days in controls, 50% lethality for PA at 11 days versus 31 days in controls).

Expression of rhea^HM05161 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.

Adults expressing rhea^GD12050 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.