Expression of mid^{dsRNA.Scer\UAS} under the control of Scer\GAL4^twi.PG results in a dramatic increase in the rate of pacing-induced heart arrest/fibrillation, with further increases with age. Down-regulation of mid also results in a severely truncated lifespan.

Heart-specific knockdown of mid through expression of mid^{dsRNA.Scer\UAS} under the control of Scer\GAL80^ts.αTub84B;Scer\GAL4^tin.CΔ4 or Scer\GAL80^ts.αTub84B;Scer\GAL4^how-24B results in an increased rate in pacing-induced heart arrest/fibrillation compared to control flies. The regularity of the myofibrillar alignment and the spacing between the Z-lines is disrupted with the tin-positive myocardium, where mid expression is diminished, but not in the ventral longitudinal muscle fibers that do not expression tin. No notable change in cell death is observed. There is a moderate decrease in diastolic diameter and a mild increase in systolic diameter in mid knockdown flies, resulting in a significant decrease in fractional shortening compared to controls.

Almost one quarter of stage 16/17 embryos expressing mid^{dsRNA.Scer\UAS} throughout the mesoderm, under the control of both Scer\GAL4^how-24B and Scer\GAL4^twi.PG, show defects in heart tube morphogenesis. These embryos exhibit intercalation, clustering and misorientation of myocardial cells. Expression of mid^{dsRNA.Scer\UAS} in differentiating myocardial cells, driven by Scer\GAL4^tin.CΔ4, disrupts the polarity of myocardial cells but does not affect their specification.

Scer\GAL4^how-24B, Scer\GAL4^twi.PG, mid^RNAi.UAS has embryonic/larval heart phenotype, enhanceable by H15^nmr-614

Scer\GAL4^how-24B, Scer\GAL4^twi.PG, mid^RNAi.UAS has dorsal vessel wall cell phenotype, enhanceable by H15^nmr-614

H15^nmr-614, Scer\GAL4^how-24B, Scer\GAL4^twi.PG, mid^RNAi.UAS has dorsal vessel wall cell phenotype

H15^nmr-614, Scer\GAL4^how-24B, Scer\GAL4^twi.PG, mid^RNAi.UAS has embryonic pericardial cell | increased number phenotype