Amino acid replacement: G1021R.
The G1021R missense mutation is in the second RING finger, predicted to reduce ubiquitin ligase activity.
G19041034A
G1021E | mib2-PA; G1021E | mib2-PB; G1021E | mib2-PC
G1021E
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
mib2S1456 homozygotes are viable.
mib2S1456 homozygous late stage 16 embryos show a small number of detached somatic muscles, but normal midgut morphology, as compared to controls; mib2S1456 homozygotes transheterozygotes present a highly penetrant complete loss of dorsal longitudinal muscles and a moderate loss of dorsal ventral muscles, whereas mib2S1259/mib2S1456 transheterozygotes maintain part of the dorsal longitudinal musculature in some cases and exhibit only mild dorsal ventral muscles defects, as compared to controls; in both these mutant combinations, the development of dorsal lateral muscles appears normal during larval and early pupal stages, but becomes defective at late pupal stages, as nascent muscles round up and eventually disappear during either template compaction or at the beginning of myofiber maturation and growth; these mutants do not show any obvious defects in larval abdominal dorsal muscle persistence, and the regeneration of both dorsal longitudinal muscles and dorsal ventral muscles still occurs.
mib2S1456 homozygous and mib2S1456/mib2S1259, mib2S1456/mib2S0768, and mib2S1456/mib2S2616 transheterozygous adults present a fully (or nearly fully) penetrant flightless phenotype, as compared to controls; mib2S1456 homozygotes and mib2S1259/mib2S1456 transheterozygous adults also present wing posture defects, which consist mostly of a held-up phenotype, and occasionally a held-down phenotype, as compared to controls; mib2S1456 homozygous adults do not show walking or climbing defects, as compared to controls.