Expression of usphs.PO using a single 30 minute 37oC heat pulse during the first larval instar stage is sufficient to rescue more than 70% of usp4 animals to the third instar stage. These rescued animals often wander only a short distance from the food near the end of the third instar stage.
Homozygous clones in the eye imaginal disc that lie posterior to the morphogenetic furrow have an abnormal arrangement of developing photoreceptor clusters. The clusters are irregularly spaced and differentiate prematurely, although they contain the normal number of cells. Movement of the morphogenetic furrow is accelerated where it passes through a homozygous clone. This displacement of the furrow is not caused by excess proliferation of usp4 cells in the clone.
Heterozygotes display thoracic defects ranging from mild, slight separation of the microchaetes and macrochaetes along the dorsal midline, to severe, a cleft extending through both the notum and scutellum. Flies also have bent and misshapen sensory bristles and develop severely knarled legs.
Females with usp mutant germ cells give rise to fully viable and fertile female usp mutant heterozygotes, but non-viable usp mutant/Y males. Most of these males die just prior to hatching, with the rest dying shortly after. The unhatched embryos have cuticular scarring in the region posterior of A9. In contrast usp mutant/Y males derived from germ cells with functional usp hatch and die between the first and second instar periods, with no gross cuticular defects. usp4 mosaic females mutant in the germline lay very few unfertilised eggs, in contrast to usp4 homozygous females (mutant both soma and germline), indicating that the fertilisation defect in these homozygotes is due to lack of usp in the soma.
Lethality occurs during embryonic and larval stages. Phenotype of homozygous germ line clones is maternal effect lethal.
Homozygous usp4 germline generates misshapen eggs.