The expression of CCT7^GD13899 under the control of either Scer\GAL4^tin.CΔ4 or Scer\GAL4^HCH.Hand leads to a severe decrease in lifespan and leads to a severe decrease in lifespan and leads to a severe decrease in lifespan and leads to near or fully penetrant cardiac defects, respectively, namely morphological defects, non-beating heart segments and non-beating hearts, as compared to controls.

The expression of CCT7^GD13899 under the control of Scer\GAL4^tin.CΔ4 also leads to progressive cardiac dysfunction, as shown by significant increases in heart period, arrhythmia, and diastolic and systolic intervals, and by significant decreases in fractional shortening, and diastolic and systolic diameter, as compared to controls. These hearts show a severe and progressive disorganization in the actin- and myosin-containing myofibrils, as compared to controls.

Expression under the control of Scer\GAL4¹⁴⁰⁷ results in shorter neuroblast lineages (less daughter cells per neuroblast) in the larval brain compared to controls.

Expression under the control of Scer\GAL4¹⁴⁰⁷ results in mild defects in the shape of neuroblasts in the larval brain.

Adults expressing Tcp-1η^GD13899 under the control of the cardioblast-specific Scer\GAL4^tin.CΔ4 driver show significantly reduced survival on day 6 after a shift to 29[o]C compared to control flies.

Adults expressing Tcp-1η^GD13899 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.

Expression under the control of Scer\GAL4^Mef2.PR results in early larval lethality.

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

Expression under the control of Scer\GAL4^Mef2.PR results in sarcomeres with reduced Z-lines in the larval body wall muscles.

Expression under the control of Scer\GAL4^pnr-MD237 results in lethality before the pupal stage.