scu^A clones in mosaic early third instar larval fat bodies do not show defects in cell size compared to controls; these cells do not accumulate autophagosome-like structures (Atg8a-positive), as compared to controls.

scu^A homozygote mutants display delay in pupariation compared to heterozygote sibling controls and although majority of the mutant animals does pupariate eventually, they all fail to eclose and survive to adulthood. High proportion of scu^A mutants also show pupal case defects - incomplete or failed spiracle eversion.

scu^A homozygous mutants display mitochondrial morphology defects in larval brain neuroblasts: the mitochondria are larger and swollen and often have ring-like shape.