l(2)efl^GD11341 driven by Scer\GAL4^Mef2.PR leads to muscle morphology defects (muscle splitting, sometimes associated with altered muscle attachments or complete loss of muscle) and sarcomere organization defects (irregular or reduced actin patterns, gaps in Z-bands) in third instar larvae, compared to wild type; there is no significant change in sarcomere size but sarcomere number is significantly decreased in ventral longitudinal muscle 3, ventral longitudinal muscle 4 and segment border muscle. Muscle defects in third instar larvae are not due to apoptotic events.

Myonuclei are irregularly distributed along muscle fibers and mitochondria are morphologically abnormal (swelling, broken cristae, glycogen deposits) in third instar larvae with l(2)efl^GD11341 driven by Scer\GAL4^Mef2.PR.

Third instar larvae with l(2)efl^GD11341 driven by Scer\GAL4^Mef2.PR have locomotor defects (increased travel time over a given distance, increased time needed for the larva to right itself from the dorsal to ventral position, fewer peristaltic movements whilst crawling) compared to wild type; the contractility index (length of relaxed versus contracted muscle fibers) is significantly decreased in ventral longitudinal muscle 3, ventral longitudinal muscle 4 and segment border muscle.

l(2)efl^GD11341 driven by Scer\GAL4^Mef2.PR leads to increased mortality during development (during larval, pupal and imago stages).

Expression of l(2)efl^GD11341 driven by Scer\GAL4^Hand.PA leads to accelerated but rhythmic heart rate (significantly reduced heart period and systolic and diastolic intervals, significantly increased systolic diameter) in adult hearts compared to wild type. l(2)efl^GD11341/+ significantly decreases systolic intervals compared to wild type.

Adults expressing l(2)efl^GD11341 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.