UAS regulatory sequences drive expression of an inverted repeat.
The expression of cherJF02077 under the control of Scer\GAL4Mef2.PU leads to significant decrease in adult viability and to a flightless phenotype, associated with defects in adult indirect flight muscles, namely shredding of myofibrils, severe decrease in the number of recognizable sarcomeres, widened or smaller/fractured Z-disc and actin incorporation into the H-zone, as compared to controls; the severe defects in sarcomere structure are enhanced by the additional expression of cherKK107518.
Expression of cherJF02077 under the control of Scer\GAL4elav.PLu in embryos leads to increased frequency of defasciculation defects in intersegmental nerve b motor axons compared to controls.
Scer\GAL4Mef2.PU, cherJF02077 has partially lethal - majority live phenotype, enhanceable by sls1/sls[+]
Scer\GAL4Mef2.PU, cherJF02077 has partially lethal - majority live phenotype, enhanceable by sls[+]/slsj1D7
Scer\GAL4Mef2.PU, cherJF02077 has myofibril | adult stage phenotype, enhanceable by sls1/sls[+]
Scer\GAL4Mef2.PU, cherJF02077 has sarcomere | adult stage phenotype, enhanceable by sls1/sls[+]
Scer\GAL4Mef2.PU, cherJF02077 has myofibril | adult stage phenotype, enhanceable by sls[+]/slsj1D7
Scer\GAL4Mef2.PU, cherJF02077 has sarcomere | adult stage phenotype, enhanceable by sls[+]/slsj1D7
The semi-lethality and the myofibril shredding defects resulting from the expression of cherJF02077 under the control of Scer\GAL4Mef2.PU is enhanced by heterozygosity for either sls1 or slsj1D7, even leading to the loss of the sarcomere structure.