domeG0468 mutants exhibit abnormal spiracles due to a lack of cell elongation.
Mutant animals are lethal at the first instar larval stage and show a phenotype in the gastrointestinal tract indicate by a block of food passage at the defective proventriculus organ. A failure of ectodermal cells to invaginate and a disorganised endodermal layer of the proventriculus is seen.
Lethality occurs during the first larval instar.
The shape of the posterior spiracles is abnormal in mutants; the stigmatophore does not protrude and only the most external part of the filzkorper is formed.
domeG0468 is a suppressor | partially of visible phenotype of upd1GMR.PB
domeG0468 is a suppressor | partially of size defective | adult stage phenotype of upd1GMR.PB
domeG0468 is a suppressor | partially of eye phenotype of upd1GMR.PB
Df(2L)32FP-5, ctdb7, domeG0468 has embryonic/larval spiracle phenotype
Df(2L)32FP-5, ctdb7, domeG0468, ems2 has embryonic/larval spiracle phenotype
In ctdb7, domeG0468, Df(2L)32FP-5 (deficiency for sal) triple mutants, no obvious spiracle structures remain, but the trachea still joins to the outside.
Quadruple ctdb7, Df(2L)32FP-5 (deficiency for sal), ems2, domeG0468 mutants are missing spiracle structures completely.
The enlarged eye phenotype seen in flies carrying one copy of upd1GMR.PB is moderately suppressed by domeG0468.
Mobilisation of the P-element reverts both the lethality and posterior spiracle phenotype.