Animals carrying Gl^t.hs and exposed to a heat shock once per day during the embryonic and larval stages develop mild posterior paralysis by the late third instar stage (penetrance of the phenotype is approximately 50%) and axonal swellings that contain retrograde and anterograde proteins (penetrance of the phenotype is 100%).

Heat induced expression causes a significant transient increase in the number of mitotic cells in the eye discs at 3, 4 and 5 hours following heat shock. Expression also causes a band of cell death behind the morphogenetic furrow and few misplaced nuclei. 1 hour heat shock of third instar larvae causes a dorsal-ventral band of defective ommatidia two or three rows wide in adult eyes. The band moves anteriorly with later heat shocks. Heat shock at early third instar shows a band of defective ommatidial cluster that exhibit nuclei mispositioning (these photoreceptors subsequently fail to differentiate) and abnormal differentiation of R1 and R6. Shorter heat shocks produce milder defects, 20 minutes is the shortest heat shock that results in mispositioned nuclei and missing cells. A 15 minute heat shock shows a clear stripe of cell death behind the furrow. Cell death is tissue and stage specific, wing or leg discs do not show increased cell death nor do heat shocked pupal eyes. Heat shock before rhabdomere development, at 37% of pupal development, causes wide irregular rhabdomeres not restricted to their normal subdomains seen later in pupal development and fused and bifurcated rhabdomeres in adults.