Flies overexpressing hhScer\UAS.cIa under the control of Scer\GAL4Hml.Δ in the hemocytes develop normally, with no obvious defects after they hatch. Expression of hhScer\UAS.cIa does not protect against infection with group B streptococcus.
Expression of hhScer\UAS.cIa, under the control of two copies of Scer\GAL4sim.PS, causes cell death in embryos.
Expression of hhScer\UAS.cIa, under the control of Scer\GAL4sca-537.4, abolishes the formation of the anterior commissure, but not of the posterior commissure. The differentiation of midline glia and MP1 neurons is also affected.
hhScer\UAS.cIa expression in all midline cells from late stage 9, driven by Scer\GAL4sim.PS, results in a severe reduction in cell number. The few remaining axons of the surviving midline cells suggest that the UMI and VUM interneurons are still able to differentiate.
When cells expressing hhScer\UAS.cIa, under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16, are transplanted close to the midline, the differentiation of MP1 neurons is disrupted. The resulting lack of MP1 axons causes a gap in the MP1 axon fascicle. In some embryos, axons project randomly across the longitudinal tracts. The number of midline cells in the affected neuromeres is not reduced, although the midline glia are occasionally absent or pushed out of the CNS. The axons of the VUM interneurons defasciculate slightly. All other midline cell lineages develop normally.
Overexpression of hhScer\UAS.cIa under the control of Scer\GAL4lz-gal4 behind the morphogenetic furrow results in mildly disordered bristles and ommatidial packing. The pupal retinas show mild defects near one edge, with occasional loss or excess cone cells (4%), mis-oriented of incompletely wrapped primary cells (44%) and excess lattice cells (55%). Photoreceptor differentiation, assessed by counting rhabdomeres in pupal retinas, is unaffected in these mutants.
The cuticles formed by hhScer\UAS.cIa; Scer\GAL469B embryos have reduced denticle diversity: rows 3-5 adopt row 2 identity (there is often an extra row 2 in addition to these), while row 6 adopts row 1 identity.
When hhScer\UAS.cIa is driven by Scer\GAL469B in the embryo a mirror image duplication of anterior denticles is seen in the abdominal area. The amount of naked cuticle seen is reduced compared to wild-type.
Expression of hhScer\UAS.cIa under the control of Scer\GAL4h-1J3 results in germ cell migration defects in the embryo. These defects are evident just after the germ cells leave the posterior midgut; instead of migrating dorsally towards the overlying mesoderm, some germ cells in stage 10-11 embryos remain associated with the posterior midgut or migrate in the opposite direction towards the ventral side of the embryo. In stage 13 embryos, germ cells are seen at a variety of abnormal positions in the posterior ectoderm in addition to the normal cluster of germ cells in the mesoderm near the posterior of the embryo. Expression of hhScer\UAS.cIa under the control of Scer\GAL4elav.PLu results in abnormal germ cell migration patterns in the embryo. Two clusters of germ cells on either side of the ventral midline can be seen in these embryos at stage 13, but in contrast to wild-type embryos the cells within the clusters are not tightly associated with each other and some are dispersed at distant sites in the posterior mesoderm. In addition, some germ cells are typically found near the ventral midline in the region just underlying the central nervous system. Expression of hhScer\UAS.cIa under the control of Scer\GAL4twi.PG results in germ cell migration defects in the embryo. In these embryos at stage 12-13, germ cells are found in several small clusters of 3-6 cells scattered in different segments along the anterior-posterior axis. In stage 14-15 embryos, many of the germ cells are clustered near the very posterior of the embryo. Expression of hhScer\UAS.cIa under the control of Scer\GAL4how-24B results in germ cells congregating in the region of the mesoderm just posterior to the midgut invagination (the site of ectopic hh expression) in stage 11 embryos.
Embryos in which hhScer\UAS.cIa is expressed under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16 have a deranged overall morphology, but the tracheal cells are capable of forming all the branches except the dorsal branch. The morphology of the branches is slightly affected but primary patterning proceeds normally. Embryos in which hhScer\UAS.cIa is expressed under the control of Scer\GAL4btl.PS have almost normal branching of the primary and secondary tracheal branches, with occasional defects in the dorsal branch and lateral trunk posterior. Excess terminal cells and excess terminal branching are seen in the dorsal branch.
Embryos expressing hhScer\UAS.cIa under the control of Scer\GAL4prd.RG1 show mutant phenotypes in every other segment. Thoracic and the first abdominal segment are principally covered by naked cuticle, while abdominal segments 3, 5 and 7 show mirror image duplication of their denticle belts, showing duplication of denticle rows 1 and 2.
When expression is driven by Scer\GAL4en-e16E the denticle belts are affected such that there is an excess of small denticles, of type row 2-4, at the expense of rows 5 and 6.
Flies expressing hhScer\UAS.cIa under the control of Scer\GAL4en-e16E show anterior displacement of wing vein 3 and a more anterior restriction of the double row bristles, leading to an expansion of the intervein 3-4 region.
Scer\GAL430A driven expression causes dramatic respecification of the pupal wing anterior compartment, costa is eliminated and triple row bristles are present on most of the anterior wing margin are replaced by double row bristles. Pupae also exhibit duplication of notal structures. Scer\GAL434B driven expression causes suppression of the costa and overgrowth in the anterior wing compartment resulting in a bulge in the anterior margin and an increase in the distance between veins II and III.