Most Prat^12A19/Df(3R)dsx43 animals arrest just prior to eclosion, although some arrest at stage P10, with patches of necrotic tissue on the wing and legs.

A few Prat^12A19/Prat^16A6 and Prat^16A6/Df(3R)dsx43 adults escapers survive. Prat^12A19/Prat^16A6 and Prat^16A6/Df(3R)dsx43 female adults have a significantly shorter life span than wild-type flies. One-half of the mutant population die within the first week, while the other half show a wider distribution of life span. Heterozygous females have a reduced mean life span compared to wild-type flies, while maximum life span is almost unaffected. The progeny of Prat^12A19/Prat^16A6 or Prat^16A6/Df(3R)dsx43 females crossed to wild-type males show strongly reduced embryonic and adult survival on normal food. There is a partial rescue of this reduced survival when the food is supplemented with RNA (the rescue of adult survival is not significant but the observed effect is in the expected direction), although the rate of egg production and the number of eggs produced does not differ between the two food types. Prat^16A6/Df(3R)dsx43 females show a number of egg chamber defects at stage 9-10 (54.7% of egg chambers are normal); 18.4% of egg chambers have multiple layers of follicle cells and border cell migration and localisation are abnormal, 11.6% have pycnotic nurse cell nuclei and the follicle cells migrate into the oocyte, 8.5% of cysts are disorganised such that the oocyte is not at the posterior pole of the egg chamber and the follicle cell layer is incomplete and 6.7% of egg chambers have an increased number of oocytes and nurse cells because two cysts are present in one egg chamber. Prat^12A19/Prat^16A6 females show a number of egg chamber defects at stage 9-10 (63.6% of egg chambers are normal); 7.9% of egg chambers have multiple layers of follicle cells and border cell migration and localisation are abnormal, 14.9% have pycnotic nurse cell nuclei and the follicle cells migrate into the oocyte, 2.2% of cysts are disorganised such that the oocyte is not at the posterior pole of the egg chamber and the follicle cell layer is incomplete and 11.4% of egg chambers have an increased number of oocytes and nurse cells because two cysts are present in one egg chamber. Embryos derived from Prat^12A19/Prat^16A6 females mated to wild-type males show defects in the early nuclear divisions, that become apparent after cycle 7. The defects seen in mutant cycle 7-13 embryos include; 17.7% of embryos show a delay in the loss of the polar body, 4.3% have chromosome bridges, 13.8% have increased yolk DNA with a normal distribution of nuclei at the blastoderm periphery, 4.6% have increased yolk DNA and nuclear gaps at the blastoderm periphery, 4.6% show desynchronisation of mitosis along the anteroposterior axis, 2.6% show desynchronisation of mitosis along the dorsoventral axis 15.7% of embryos are unfertilised (36.7% of mutant cycle 7-13 embryos appear normal). Embryos derived from Prat^16A6/Df(3R)dsx43 females mated to wild-type males show defects in the early nuclear divisions, that become apparent after cycle 7. The defects seen in mutant cycle 7-13 embryos include; 23.9% of embryos show a delay in the loss of the polar body, 5.3% have chromosome bridges, 14.2% have increased yolk DNA with a normal distribution of nuclei at the blastoderm periphery, 3.5% have increased yolk DNA and nuclear gaps at the blastoderm periphery, 4% show desynchronisation of mitosis along the anteroposterior axis, 2.2% show desynchronisation of mitosis along the dorsoventral axis 17.5% of embryos are unfertilised (27.4% of mutant cycle 7-13 embryos appear normal). Late stage embryos derived from Prat^16A6/Df(3R)dsx43 females mated to wild-type males show defects in segmentation of the cuticle with a stronger effect on late-stage embryos than on first instar larvae. The most common defect in embryos is segmental fusion which covers all the abdominal segments or the segments from A3 to A6. Other weaker segmental fusions are present in first instar larvae, which involve a modification of the segmentation around A4, with different degrees of severity of fusion. Rarer defects include absence or a decrease in the size of the A4 segment and its misplacement along the anterior-posterior axis, and an alteration of the lateral part of the A4 segment, so that the cuticle is disrupted and the remaining lateral part is no longer aligned with the ventral part.

Reduced viability, and posterior crossvein gap phenotype.