With a normal diet, (all percentages approximate) 80% of Df(3R)Fer/Df(3R)Fer mutant embryonic cuticles are similar to wild type, 1% have dorsal closure defects, 1% have germ band retraction defects, 9% have head involution defects and 9% have no cuticle deposition. Ferritin expression and iron availability in adults is reduced via an iron-specific chelator (Bathophenanthroline Sulfate, BPS) in the diet, leading to decreases in ferritin/iron maternal contribution to embryos and enhancing embryonic cuticle defects: 50% are similar to wild type, 15% have head involution defects, 6% have dorsal closure defects, 4% have germ band retraction defects and 25% have no cuticle deposition. Feeding extra iron (high iron diet) to adults does not rescue zygotic embryonic cuticle phenotypes in mutant offspring: 75% are similar to wild type, 5% have head involution defects, 2% have dorsal closure defects and 18% have no cuticle deposition. Df(3R)Fer/Df(3R)Fer embryos have significantly different abnormal central nervous systems compared to controls: they appear twisted, disorganized, ventral nerve cords often have holes of variable size and number; brains are also disrupted. Df(3R)Fer/Df(3R)Fer embryos have significantly different abnormal central nervous systems compared to controls: they appear twisted, disorganized, ventral nerve cords often have holes of variable size and number; brains are also disrupted, along with defects in neuroblasts and ganglion mother cells and disorganized axons from CNS ventral nerve cord. Ectopic apoptotic activation appears in Df(3R)Fer/Df(3R)Fer embryos at stage 12 (none detected in wild type), with massive apoptosis by stage 15 (compared to weak restricted signals in wild type).
