43% of Fer1HCH⁰⁰⁴⁵¹/Fer1HCH⁰⁰⁴⁵¹ mutant embryos die during embryogenesis. With a normal diet, (all percentages approximate) 65% of mutant embryonic cuticles are similar to wild type, 2.5% have dorsal closure defects, 2.5% have germ band retraction defects, 10% have head involution defects and 20% 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, 20% have head involution defects, 3% have dorsal closure defects, 2% 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, 1% have dorsal closure defects, 1% have germ band retraction defects and 18% have no cuticle deposition. Consistent with early ferritin/iron requirements during embryogenesis, mutant germline clones have severe embryonic cuticle phenotypes: 5% are similar to wild type, 12% have head involution defects, 5% have dorsal closure defects, 3% have germ band retraction defects and 75% have no cuticle deposition.

Fer1HCH⁰⁰⁴⁵¹/Fer1HCH⁰⁰⁴⁵¹ 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 Fer1HCH⁰⁰⁴⁵¹/Fer1HCH⁰⁰⁴⁵¹ embryos at stage 12 (none detected in wild type), with massive apoptosis by stage 15 (compared to weak restricted signals in wild type).

The lethality seen in homozygous or hemizygous Fer1HCH⁰⁰⁴⁵¹ mutants cannot be rescued by the addition of iron.

Fer1HCH⁰⁰⁴⁵¹ mutants grow to mid-first instar after hatching and then stop growing. They are arrested at this stage but survive for approximately 7 days before dying.

Fer1HCH⁰⁰⁴⁵¹ mutant larvae show diminished BrdU incorporation and triacylglycerol levels 18hrs after hatching, as found in starved wild-type flies.

Females carrying homozygous germline clones are fertile.

Homozygous clones in the adult germ cells do not result in defects in the fusome.

Fer1HCH^G00188/Fer1HCH⁰⁰⁴⁵¹ has lethal phenotype, non-suppressible by Scer\GAL4^Act.PU/Fer2LCH^UAS.cMa

Fer1HCH⁰⁰⁴⁵¹ has lethal phenotype, non-suppressible by Scer\GAL4^Act.PU/Fer2LCH^UAS.cMa