Somatic clones expressing EgfrDN.UAS.cBa under the control of Scer\GAL4Tub.PU contain a smaller overall number of cells and intestinal stem cells in adult flies compared to controls, but maintain a wild-type ratio of stem cells/clone.
Adulthood-generated midgut clones expressing EgfrDN.UAS.cBa under the control of Scer\GAL4Tub.PU have significantly fewer cells, but insignificant changes in the number and proportion of intestinal stem cells, as compared to control clones.
Expressing EgfrDN.UAS.cBa under the double control of Scer\GAL4twi.2PE and Scer\GAL4how-24B leads to embryos showing severely decreased numbers of cardioblasts, namely of generic cardioblasts, leading to a lower generic CBs:ostial CBs ratio than the typical 4:2 ratio.
Expressing EgfrDN.UAS.cBa under the control of Scer\GAL4twi.2PE leads to embryos showing a significant decrease in the number of odd pericardial cells, although even pericardial cells are unaffected, as compared to controls.
Expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4C587 (in combination with Gal80[ts] to restrict expression to adulthood) leads to a substantial increase in the number of germline stem cells in the germinal proliferation center, as compared to controls.
Expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4repo.PL (and using tub-Gal80[ts] to restrict the expression to larval stages) result in significantly reduced axon wrapping index (proportion of axon clusters wrapped by wrapping glia) and many axons are wrapped in abnormally large fascicles, expression under Scer\GAL4nrv2.PS also reduces the wrapping index but the number of wrapping glial cells along the nerve is unchanged whereas the number of perineurial glial cells is robustly decreased in third instar larvae.
In wild-type larvae, subperineurial glial cells (SPGs) form autocellular contacts with pronounced septate junction, the length of these autocellular contacts is significantly reduced upon Scer\GAL4moody.SPG-driven (in SPGs) knock-down of vn.
Larvae expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4n-syb.PS show a significantly lower learning index compared to control larvae in an olfactory learning assay. These larvae show normal gustatory preference responses to fructose and to quinine and show normal olfactory responses to amyl acetate and to 1-octanol.
Expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4elav.Switch.PO for just 24 hours in late larval stages (using mifepristone to control the timing of expression) results in significantly reduced olfactory learning ability in larvae.
Larvae expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4ey-OK107 show a significantly lower learning index compared to control larvae in an olfactory learning assay.
Expression of under the control of Scer\GAL4Dl-05151-G (and using tub-Gal80[ts] to limit the stage of expression) diminishes the increase in the rate of intestinal stem cell division normally observed in the adult midgut upon bacterial infection challenge. This effect is not seen when EgfrDN.Scer\UAS.cBa is expressed under the Scer\GAL4esg.PU driver (with tub-Gal80[ts]).
Expression of EgfrDN.Scer\UAS.cBa in stage 16 embryos, under the control of Scer\GAL4neur-GAL4-A101 results in the loss of vdaB in 75% of parasegments. There is no loss of v'ada. Examination of stage 12 embryos reveals that vdaB-loss is preceded by SOP1a loss in 78% of cases. SOP4a are not affected.
Induction of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4wg-IS650 during 0-30 hours after pupal formation blocks apoptosis and rearranges the wing margin cells. In addition, blocking ecdysone signalling results in overlap of the double-row hairs in the adult wing.
Expression of EgfrDN.Scer\UAS.cBa in intestinal stem cells (ISCs) driven by Scer\GAL4esg-NP5130 and Scer\GAL80ts.αTub84B does not significantly affect the number of ISCs in the gut. However, in sharp contrast to wild-type flies, Erwinia carotovora carotovora 15 (Ecc15) infection does not increase the number of intestinal mitotic cells.
Guts from flies expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4Myo31DF-NP0001 are almost double the length and half the width compared with the guts of wild-type flies. However, the total number of enterocytes is the same as it is in wild-type controls. The alteration in gut length correlates with changes in the shape of enterocytes. In contrast to wild-type enterocytes, the mutant enterocytes appear flattened and lack the extension of their apical domain. In addition, the distance between nuclei of neighbouring enterocytes (indicative of epithelial density) increases twofold in these flies and altered in its axis. This effect on cell shape is more pronounced in certain gut segments, particularly around the copper cell region which is normally composed of a highly polarised columnar-type epithelium and is folded within the abdomen. As a consequence, guts of flies expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4Myo31DF-NP0001 are long and thin in this region and lack their characteristic folding.
Flies expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4Myo31DF-NP0001 succumb within 48 hours after ingesting Erwinia carotovora carotovora 15 (Ecc15). This increased susceptibility is associated with a rupture in gut integrity, as indicated by the presence of bacteria in the hemolymph.
Guts of flies overexpressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4Myo31DF-NP0001 and Scer\GAL80ts.αTub84B shifted to the restrictive temperature for 4 to 5 days are initially of normal size. A significant increase in gut length is observed when flies are incubated for 3 weeks at the restrictive temperature.
Guts of flies overexpressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4Myo31DF-NP0001 and Scer\GAL80ts.αTub84B are 20% longer compared with guts wild-type flies 48 hours post-infection with Erwinia carotovora carotovora 15 (Ecc15).
Guts of flies expressing EgfrDN.Scer\UAS.cBa in enterocytes under the control of Scer\GAL4Myo31DF-NP0001 and Scer\GAL80ts.αTub84B shrink less upon infection with Erwinia carotovora carotovora 15 (Ecc15). After a recovery phase of 2 or 8 days, the guts are 25% longer than their wild-type counterparts.
In contrast to wild-type flies, cell blebbing, the multi-layering of enterocytes or loss of cells into the lumen of flies are not observed in flies expressing EgfrDN.Scer\UAS.cBa in enterocytes under the control of Scer\GAL4Myo31DF-NP0001 and Scer\GAL80ts.αTub84B. In sharp contrast to wild-type enterocytes, apoptotic enterocytes with fragmented nuclei are observed within the epithelium of flies expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4Myo31DF-NP0001 and Scer\GAL80ts.αTub84B.
Embryos expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4twi.PG show a decrease in the number of dorsolateral and lateral adult muscle precursor cells compared to wild type.
Expression of EgfrDN.Scer\UAS.cBa in the anterior cells of the egg chamber, under the control of Scer\GAL455B, results in eggs with a single fused dorsal appendage or with a patch of dorsal appendage material.
Expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4ems.HRE impairs filzkorper formation but does not affect stigmatophore formation. However, expression of this transgene under the control of Scer\GAL4salm-459.2 has the reciprocal effect; stigmatophore formation is impaired while filzkorper formation is unaffected.
The number of macrochaetae/heminotum in animals expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4ap-md544 is - anterior+posterior notopleural: 1.61, presutural: 0.70, anterior supraalar: 0.50, posterior supraalar: 0, anterior postalar: 0, posterior postalar: 0, anterior+posterior dorsocentral: 0.78 and anterior+posterior scutellar: 1.55.
When expression is driven by Scer\GAL4ap-md544 most notum macrochaetae are removed, though microchaetae are unaffected.
Embryos expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4twi.PG show loss of VA2 muscle precursor cells (only 26% of hemisegments contain VA2 precursor cells).
Expression of EgfrDN.Scer\UAS.cBa can result in loss of sensory organs in the ocellar sensory system (OSS), unless raised at 17oC, which allows some differentiation of these neurons. In these conditions, some axon guidance defects are seen in OSS neurons. The most common alteration (in about 1/3 of animals) is bristle mechanosensory (BM) axons stalling in the epidermis. Alterations in Ocellar pioneer (OP) axon guidance are much less frequent.
Expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4Gsc-SNS1 results in suppression of the formation of the anterior most invagination fold in the stomatogastric nervous system anlage, without affecting the others, in stage 11 embryos.
When expressed under the control of Scer\GAL4c591, the ocelli and the ocellar bristles are deleted. However, most of the interocellar cuticle is retained.
Expression of EgfrDN.Scer\UAS.cBa driven by Scer\GAL4Bx-MS1096 deletes parts of dorsal veins L3, L5 and the distal portion of L4, reduces the width of the wing, and causes mis-alignment between dorsal and ventral components of the veins.