Amino acid replacement: G277E.
The G277E missense mutation is in the first Mib-specific domain (MIB).
G19038679A
G277E | mib2-PA; G277E | mib2-PB; G277E | mib2-PC
G277E
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
mib2S1259 homozygotes are viable.
mib2S1259 homozygous late stage 16 embryos show a small number of detached somatic muscles, but an apparently normal midgut morphology, as compared to controls; mib2S1259 homozygous adults present a fully penetrant and complete loss of dorsal longitudinal muscles and a severe loss of dorsal ventral muscles, whereas mib2S1259/mib2S1456 transheterozygous adults maintain part of the dorsal longitudinal musculature in some individuals and exhibit only mild dorsal ventral muscle 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; both 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.
mib2S1259 homozygous and mib2S1259/mib2S1456, mib2S1259/mib2S0768 and mib2S1259/mib2S2616 transheterozygous adults present a fully (or nearly fully) penetrant flightless phenotype, as compared to controls; mib2S1259 homozygous 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; mib2S1259 homozygous adults do not show walking or climbing defects, as compared to controls.
mib2S1259/Df(2L)Exel8039 transheterozygous adults present a severe loss of dorsal ventral muscles, as compared to controls.
