Homozygous larvae reach the third larval stage with a 6-hour delay and do not exhibit significant size differences relative to wild-type. Larvae enter pupariation with a 3-day delay. Most die as pharate adult. The few escapers are reduced in body weight (26%) and total wing area (6%). The wing cell area is strongly reduced by 22%. However overall larval growth is not impaired in 5-day old larvae. Larval tissues in mutants normal. The endoreplicative cells of the larval gut are of normal size. However, mutant midguts 5 days after egg laying (AEL) has fewer isolated intestinal adult precursor cells (apc) than wild-type. They are usually seen as doublets or occasionally as groups of 3-4 cells (as opposed to 4-8 cells in wild-type). In addition mutant apc appear to be smaller than wild-type. Proliferation is not arrested however, since apc eventually form groups of 4-8 cells in 7 days AEL mutant larvae. Mutant wing imaginal discs are severely delayed in growth. However at the extended third instar (7-8 days AEL), the mutant discs attain a size comparable to prepupal wild-type discs. The reduced growth rate is not due to an enhancement of cell death, as no increase of apoptotic cells is observed. The cell cycle profile of mutant prepupal wing discs is normal, but a reduction in size in G1 and G2 cells.
100% of modL8/mod07570 males are sterile. modL8 animals (in which the krzL8 phenotype of the Df(3R)A4-4L8 deficiency has been rescued by krz+t5.8) fail to eclose and die as pharate adults. They pupate up to 7 days after their control siblings and have a distinct minute phenotype.
Homozygous clones in the head, thorax, legs and abdomen are reduced in size compared to control clones. Clones in the thorax produce short slender bristles. This phenotype is cell-autonomous.
High frequency of melanotic tumours.
Severe muscle phenotype: myoblasts retain a segmentally repeated pattern but fail to form elongated fibres and establish or maintain their insertion in the epidermis. In less severe cases myoblasts fuse and muscle fibres elongate but fail to reach the right attachment sites on the epidermis. Defects in head and tail structures. Salivary glands of mutant larva escapers exhibit gross morphological defects.