Expression of KrScer\UAS.cHa using Scer\GAL4how-24B leads to mis-arrangements and patterning defects of the somatic musculature, including reduced numbers and altered shapes of the lateral transverse (LT) muscles. The remaining LT muscles are often bent at their ventral endings and others appear thicker and shorter.
Third instar larvae expressing KrScer\UAS.cHa under the control of Scer\GAL4Pxn.PS contain an increased proportion of lamellocytes as a proportion of total hemocyte number (9.5% compared to 0.5% in controls). Hemocytes are unable to undergo phagocytosis of small particles; unlike controls, they do not engulf India ink particles, instead adhering to larger particles India ink particles.
Approximately 40% of flies expressing KrScer\UAS.cHa under the control of Scer\GAL4Pxn.PS exhibit melanotic tumours.
Expression of KrScer\UAS.cHa under the control of Scer\GAL4pros.PMG at 22oC results in each hemisegment having five to six eve+ U neurons, mostly a U1, a U2 and three U3 neurons (91%), but sometimes a U1, a U2 and four U3 neurons (9%). Expression of two copies of KrScer\UAS.cHa under the control of Scer\GAL4pros.PMG at 29oC results in extra eve+ U neurons; each hemisegment contains on average a U1, a U2, 7.8 U3 neurons and no U4/U5 neurons. Embryos expressing KrScer\UAS.cHa under the control of Scer\GAL4sca-4512 have a total number of 7 to 8 eve+ U neurons in each hemisegment, although ectopic U3 neurons range from 2 to 6 in number. Hemisegments with only two ectopic U3 neurons typically have U4/U5 neurons, those with 3 ectopic U3 neurons have only a U4 neuron and those with four or more ectopic U3 neurons lack both U4/U5 neuronal fates.
When KrScer\UAS.cHa is driven by one copy of Scer\GAL4ftz.ng a minor SNb phenotype is seen. The distal RP axons fail to reach their target muscles and maintain growth cone like structures at their ends. With two copies, a stronger phenotype is seen. In 36% of cases, the most distal RP axons stall RP5 axons does not innervate the target muscle 12. Whereas in all other cases, the SNb stalls at the second choice point. When a single copy of KrScer\UAS.cHa is driven by Scer\GAL4how-24B the RP3 axon separates properly from the SNb and finds the cleft between target muscles 7 and 6, whereas the remaining RP axons fail to defasciculate. Two copies of KrScer\UAS.cHa causes stronger defects. The SNb stalls at the position where RP3 would normally defasciculate. KrScer\UAS.cHa driven by Scer\GAL4twi.PG also gives axon guidance phenotypes in the RP axons.
When KrScer\UAS.cHa is driven Scer\GAL4en-e16E, there are extra cells in the neuroblast 7-3 lineage and all but 2 cells differentiate as GMC-2 derived interneuron 2; the two unaffected cells are the GMC-1 derived 1/1G neurons. Extra eve+ neurons are also seen in these animals, with all differentiating as U3 or U4 motorneurons, except the normal pair of early born U1/U2 motorneurons.
When KrScer\UAS.cHa is expressed under the control of Scer\GAL4ptc-559.1 in the embryonic hindgut, extra cells express ct and evert from the hindgut to produce enlarged Malpighian tubule primordia.