Insertion within the open reading frame.
36% of Fer2LCH00035/Fer2LCH00035 mutant embryos die during embryogenesis. With a normal diet, (all percentages approximate) 75% of mutant embryonic cuticles are similar to wild type, 5% 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: 35% are similar to wild type, 15% have head involution defects, 4% have dorsal closure defects, 6% have germ band retraction defects and 40% 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, 6% have head involution defects, 4% have germ band retraction defects and 15% have no cuticle deposition. Consistent with early ferritin/iron requirements during embryogenesis, mutant germline clones have severe embryonic cuticle phenotypes: 7% are similar to wild type, 9% have head involution defects, 2% have dorsal closure defects, 2% have germ band retraction defects and 80% have no cuticle deposition.
Fer2LCH00035/Fer2LCH00035 mutant 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 Fer2LCH00035/Fer2LCH00035 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 Fer2LCH00035 mutants cannot be rescued by the addition of iron.
Fer2LCH00035 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.
Fer2LCH00035 mutant larvae show diminished BrdU incorporation and triacylglycerol levels 18hrs after hatching, as found in starved wild-type flies.
l(3)00035/l(3)10605 and l(3)00035/l(3)00451: thin bristles and semi-sterile: may be weak alleles
Fer2LCH00035 has lethal | recessive phenotype, non-suppressible by Scer\GAL4Act.PU/Fer1HCHUAS.cMa
Fer2LCH00035 has lethal | recessive phenotype, non-suppressible by Scer\GAL4Act.PU/Fer1HCHmut.UAS
Fer2LCH[+]/Fer2LCH00035 is an enhancer of scutellar bristle | increased number phenotype of SsdpL7
Fer2LCH[+]/Fer2LCH00035 is a non-enhancer of scutellar bristle | increased number phenotype of Chie5.5
Fer2LCH[+]/Fer2LCH00035 is a non-enhancer of wing margin phenotype of Bx2
Fer2LCH[+]/Fer2LCH00035 is a non-suppressor of wing margin phenotype of Bx2
Fer2LCH[+]/Fer2LCH00035 is a non-suppressor of scutellar bristle | increased number phenotype of Chie5.5
Fer2LCH00035 is rescued by Scer\GAL4Act.PU/Fer2LCHUAS.cMa
Ubiquitous expression of Fer2LCHScer\UAS.cLa under the control of Scer\GAL4Act5C.PI rescues the first instar larval stage lethality seen in Fer2LCH00035 mutants.
A. Spradling.
Complements: Fer1HCH00451. Complements: tmod00848. Complements: Fer1HCH02038. Complements: Fer1HCH04693. Complements: Fer1HCH09408. Complements: Fer1HCH10605. Complements: Fer1HCHj10B4. Complements: l(3)j2D5j2D5. Complements: l(3)s2564s2564.