Heterozygous uif^2B7 mutant flies exhibit increased indirect flight muscle degeneration compare to controls.

Approximately 15% of homozygous and uif^2B7/Df(2L)Exel7029 animals die as embryos, and all those embryos that hatch die as larvae. Most homozygous larvae die as small first instar larvae, although 13% advance to the third instar stage. The mutant larvae grow much slower than their control siblings.

More than 90% of uif^2B7/Df(2L)Exel7029 dead embryos show no obvious patterning defects nor defects in morphogenesis (including germ band retraction, dorsal closure or head involution), while the remaining embryos have mild defects in head involution.

83% of homozygous dead embryos have no obvious morphological defects, while the remaining 17% have mild defects in head involution or in the head skeleton.

10% of uif^1A15/uif^2B7 animals show embryonic lethality, and all those embryos that hatch die as larvae.

Unhatched homozygous embryos and newly hatched larvae show a failure of tracheal inflation. This phenotype shows complete penetrance but variable expressivity. The junctions between inflated and non-inflated regions of the dorsal trunk do not correlate with the location of fusion between adjacent tracheal metameres. Irregularities are seen in the trachea of mutant larvae, including twists, constrictions and crumpled dorsal trunks.

The tracheal inflation defects seen in mutant larvae result from a defect in the establishment of inflated tracheae during embryogenesis and not from a defect in maintaining inflated tracheae throughout embryogenesis or into larval life.

Tracheal patterning and tube size control are normal in stage 16 homozygous embryos. The diameter and length of the dorsal trunk are normal in stage 16 homozygous embryos. Chitin is secreted into the lumen of mutant tracheal tubes and forms a continuous dense cable through the trachea at stage 16, as occurs in wild type. By stage 17, chitin has been cleared from the centre of the trachea lumen in homozygous embryos, as occurs in controls. The mutant embryos have normal paracellular barrier function in the salivary gland and tracheal epithelium (assayed using a dye permeability assay).

Mutant larvae spend very little time in the food and instead wander around the plate, even if they appear to have mostly inflated trachea (a behaviour that has been shown to be a response to hypoxia).

Homozygous second instar larvae show a tracheal moulting defect in which two tracheal cuticle layers are present with only the first instar trachea being inflated. This moulting defect is also seen in mutant third instar larvae, with at least two tracheal cuticles and occasionally three cuticular layers being seen.

uif^2B7/Df(2L)Exel7029 third instar larvae show a strong reduction in tracheal tube length.

uif^2B7/Df(2L)Exel7029 third instar larvae show a weakly penetrant defect in epidermal moulting in which the previous cuticle remains attached to the larva at its posterior spiracles.

Taenidia are present in the tracheae of homozygous third instar larvae, although their density is lower and they show some irregularities (in some cases the rows converge and appear to cross each other).

uif^2B7/uif[+] is an enhancer of indirect flight muscle cell phenotype of Dys^RNAi.NH2.UAS, Scer\GAL4^Act.PU

uif^2B7/uif[+] is an enhancer of indirect flight muscle cell phenotype of Dg^RNAi.UAS, Scer\GAL4^Act.PU

Df(3R)Exel6184/+, uif^2B7 has indirect flight muscle cell phenotype

Dg[+]/Dg^O86, uif^2B7 has indirect flight muscle cell phenotype

Dg^RNAi.UAS, Scer\GAL4^Tub.PU, uif^2B7 has indirect flight muscle cell phenotype