domeG0217 mutants show premature differentiation to P1+ plasmatocytes.
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. The proventriculus development is normal in early stages of proventriculus development in mutants. However in the keyhole stage, the anterior boundary cells fail to move inward into the endodermal keyhole domain and arrest anterior to the proventricular endoderm until late stages of embryonic development. Furthermore, the endodermal cell layer of the keyhole is disorganised and the proventriculus is collapsed.
Homozygous embryos lack filzkorper.
Lethality occurs during the embryonic stage and the first larval instar.
The shape of the posterior spiracles is affected in mutants. Homozygous embryos derived from homozygous female germline clones have segmentation defects, such as deletion of segment A5 and most of the A4 denticle belts, partial or total fusion of segments A6 and A7 and a variable reduction of the thoracic segments and A8.
The enlarged eye phenotype seen in flies carrying one copy of upd1GMR.PB is moderately suppressed by one copy of domeG0217.
Mobilisation of the P-element reverts both the lethality and posterior spiracle phenotype.