The increased relative size of somatic MARCM clones mutant for exe1 in third instar larval wing discs (as compared to wild-type clones in control discs) is suppressed by expression of kibraScer\UAS.P\T.cGa in the mutant clones (driven by Scer\GAL4tub.PU), which on its own produces clones of reduced size.
The overgrowth phenotype observed in adult eye and antennae containing exe1 homozygous mutant somatic clones (induced by the eyFLP method) is not changed when the clones are induced in Ack10b/Ack10b mutant background or when they also express AckScer\UAS.T:SV5\V5 under the control of Scer\GAL4Ubi.PU.
exe1/+ fully suppresses the reduced growth seen in posterior midgut wild type clones when in the presence of ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones, and suppresses the growth of ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones.
The supernumerary inter-ommatidial cells in the pupal retina as well as the smaller size and altered eye shape in adults characteristic for exe1/exe1 eyes (created by the EGUF method in otherwise heterozygous animals) can be suppressed by combination with ZyxΔ41/ZyxΔ41.
The low survival rate of exe1/exe1 mutants to third instar larval stage can be improved by combination with ZyxΔ41/ZyxΔ41 and some of the double mutants can survive even to adulthood. The decreased number of photoreceptor cells in the eye discs characteristic for exe1/exe1 mutants is also restored in the surviving exe1;ZyxΔ41 double mutant third instar larvae.
tai61G1/tai61G1, exe1/exe1 mosaic adult wings are smaller than exe1/exe1 mosaic wings, although the wings are still a broader shape than controls; tai61G1/tai61G1, exe1/exe1 clones in the L3 wing disc appear smaller than age-matched exe1/exe1 clones; tai61G1/tai61G1, exe1/exe1 mosaic heads have suppressed head and eye overgrowth as compared to exe1/exe1 clones.
Pupae with mosaic heads that are largely doubly mutant for exe1/exe1 and kibra1/kibra3 (clones induced using the eyFLP method without cell lethal) do not eclose and normal head structures are displaced by overgrown tissue.
dmScer\UAS.cZa overexpression clones (under the control of Scer\GAL4hh.PU) found in the posterior of the wing disc strongly enhance the proliferative activity of exe1 mutant cells. In addition these cells are larger in dmScer\UAS.cZa clones than in a wild-type background.
exe1 allows recovery of Df(1)su(s)R194/+ clones in the adult eye in animals with mosaic eyes containing two genotypes of cells with respect to RpL36; cells which are Df(1)su(s)R194/+ and cells in which the haplo-insufficiency of Df(1)su(s)R194/+ for RpL36 has been rescued by RpL36+t4 (in a wild-type background the Df(1)su(s)R194/+ clones are eliminated by cell competition and are not seen in the adult eye in these animals).
Somatic clones homozygous for Mer4 and exe1 in the antenna or in the dorsal thorax are massively overgrown. In the mid-pupal retina, these clones contain a large excess of inter-ommatidial cells. In the late third instar eye disc, cells in these clones show increased levels of mitosis after (posterior to) the second mitotic wave. Later, at around 25 hours APF, the widespread apotosis seen throughout the developing retina in wild-type and heterozygous cells, is largely suppressed in these clones.
Mer4; exe1 somatic clones in contact with the posterior or lateral margin of the eye fail to produce photoreceptors. Those somatic clones located in the middle of the eye field can produce photoreceptors.
ft8/ftG-rv exe1 mutant retinas exhibit an increase in the number of secondary cells per ommatidia (approximately 9, compared to 6 in wild-type), that is not statistically significant from ft8 single mutants.
One copy of exe1 enhances the lethality of ft8/ftG-rv animals. Those that are wild-type for exe1 but mutant for ft8/ftG-rv emerge as 0.32% of the progeny, whereas those that are also mutant for exe1 emerge as 0.269% of the progeny, a small, but statistically significant difference.
Dominantly enhances the head phenotype of Mer3 hemizygotes. Both vein and intervein cells can differentiate in Mer4; exe1 double mutant clones in the wing. Clones that intersect the position of the posterior crossvein disrupt its development. Clones in the position of the anterior crossvein develop normally. Within the mutant intervein and vein clones, apparent defects in proliferation control are seen; in the proximal region of the wing, clonal vein tissue forms a raised protrusion. In other regions of the wing, bulges in the veins are also seen, although more frequently vein clones are merely broadened when compared with the surrounding vein. In the intervein regions, the clonal tissue appears to bulge and crinkle within the confines of the normal tissue, suggesting overproliferation. Cells within the intervein clones appear to differentiate as intervein cells, however, the cuticle deposited at the base of each wing hair within the clone appears to be thickened, and is distinct from cuticle produced by either the surrounding heterozygous intervein or vein cells. Mer4; exe1 double mutant clones in the eye appear to disrupt the progression of the morphogenetic furrow, being seen either as small scars with associated clusters of bristles or as elongated scars and associated indentations running from within the eye field towards the anterior margin. These clones do not differentiate ommatidia. The clones are often associated with overproliferated head cuticle.