Mutant embryos have gaps in the dorsal trunk without ectopic branching. The tracheal cells of heterozygotes show moderate lack-of-migration defects in 68% of embryos, and show severe ectopic lack-of-migration defects in 14% of embryos.
Homozygous clones remain in the proximal region of the dorsal air sac primordium and never colonise the distal region.
Homozygous embryos show little branch migration in the tracheal system.
84% of heterozygous embryos show a tracheal lack of migration phenotype.
homozygous clones in the dorsal air sac primordium grow and divide normally but never contribute to the tip of the primordium.
In stage 14 homozygous btlH82Δ3
embryos there is very little tracheal tubule migration as compared to wild-type. The dorsal trunks of the tracheal system of stage 16 btlH82Δ3
heterozygous embryos lack many dorsal branches.
The failure of tracheal cells to migrate in btlH82Δ3
mutant embryos is accompanied by a failure of these cells to form filopodia.
Homozygous embryos show no tracheal cell migration (although tracheal cells are specified and invaginate properly), resulting in the lack of all tracheal branches.
Homozygous embryos show some inhibition of tracheal branching.
In homozygous stage 15 embryos the tracheal cells fail to migrate, remaining in a tracheal sac-like formation. Expression of btlhs.T:λ\cI-DD
in heterozygous btlH82Δ3
embryos causes dorsal trunk defects, 4 or more interruptions.
Clones in which all border cells are btl-
show no defects in border cell migration, though mild delays or low frequency defects would not have been detected.
Tracheal pits form, but tracheal cells undergo only limited migration.