Fig. 4

Identification of genes required for the survival of persistent muscles. Dorsal views of abdominal segments A2 and A3 of four genotypes are shown in five time points after head eversion in the anterior-posterior orientation from left to right. Muscles were labelled with tau-GFP (green) and histone-mKO (red). For more details, see Additional file 4: Video 1.(a) In a pupa expressing a control shRNA, persistent muscles (DIOM1) near the midline (vertical arrows) survived to adulthood, while laterally located obsolete DEOM2s (*) were fragmented into fluorescent sarcolytes that persisted into late pupation. (b) Overexpression of the dominant negative (DN) TOR (TOR ^TED) initially prevented destruction of the DEOM1s (arrow heads, +3 h aHE), which occluded the DIOMs underneath (diagonal arrows). Subsequently (+12 h, +20 h), both DEOMs and DIOMs condensed and disintegrated. (c) Gene silencing of Rm62 led to histolysis of DIOMs at +20 h. (d) Silencing of Cp1 induced degeneration of DIOMs in mid pupation from +38 to +70 h. At +43 h, the muscles in A2 completely histolysed (dashed arrows), while the DIOM1 (arrow) in the right hemi-segment of A3 disintegrated almost 20 h later. Premature cell death of the three gene perturbations was restricted to larval persistent muscles. The DIOM1 in the left hemisegment of A3 survived (+75 h, arrow). As can be seen at +75 h, none of the gene perturbations caused discernible effects on the survival of newly formed adult muscle like dorsal abdominal muscles (double arrows) or the heart (heart shape). The scale bars in (d) represent 100 μm