Response to sound, measured via compound action potentials in the antennal nerve, is disrupted in flies in which a subset of the Johnston's organ neurons has been eliminated by via Rcom\RA[Scer\UAS.cSa] driven by Scer\GAL4^JO15 + Scer\GAL4^ph-p-NP1046.

Embryos expressing Rcom\RA^Scer\UAS.cSa in the mesoderm under the control of Scer\GAL4^bap.3 show only residual migration of the endoderm.

Embryos expressing Rcom\RA^Scer\UAS.cSa in the mesoderm under the control of Scer\GAL4^miple2.PW have no visible endoderm at stage 13 and the visceral mesoderm appears disorganised.

Ablation of Johnston's organ "C" and "E" neurons via Scer\GAL4^NP6250-mediated expression of Rcom\RA^Scer\UAS.cSa eliminates the wind-induced suppression of locomotion response, whereas basal locomotor activity, phototaxis behaviour, and hearing are unaffected.

Embryos expressing Rcom\RA^Scer\UAS.cSa in the haemocytes under the control of Scer\GAL4^srp.Hemo display ventral nerve cord condensation defects.

Expression of Rcom\RA^Scer\UAS.cSa under the control of Scer\GAL4^elav.PU results in ablation of neurons in embryos, but longitudinal glia divisions that occur before axonal contact (longitudinal glioblast up to the 4-longitudinal glia stage) are unaffected.

Expression of Rcom\RA^Scer\UAS.cSa under the control of Scer\GAL4^Mz19 results in ablation of all Scer\GAL4^Mz19-expressing projection neurons (including those innervating glomeruli DA1 and VA1d) and the absence of their dendrites from the corresponding glomeruli.

Expression of Rcom\RA^Scer\UAS.cSa under the control of Scer\GAL4^Or88a.cWa or Scer\GAL4^Or47b.7.467 ablates the cell bodies (in the antenna) and axons (in the antennal lobe) of Or88a/Or47b-expressing olfactory receptor neurons (ORNs), resulting in a significant reduction in the size of their respective glomeruli (VA1d and VA1lm). After ablation of Or88a/Or47b-positive ORNs, the associated Scer\GAL4^Mz19-expressing projection neuron (PN) dendrites remain confined to their target glomeruli for up to 30 days - that is, ablation of a single ORN class does not alter the dendritic innervation pattern of PNs normally projecting to the same or a neighbouring glomerulus.

Induction of expression of Rcom\RA^Scer\UAS.cSa under the control of Scer\GAL4^Mz19 upon eclosion leads to death of Scer\GAL4^Mz19-expressing projection neurons (PNs). PN death does not appear to alter glomerular size, neither does it affect innervation of the VA1d glomerulus by Or88a-positive olfactory receptor neurons or ORN axons that project to Scer\GAL4^Mz19-negative glomeruli.

Expression of Rcom\RA^Scer\UAS.cBa in aCC and RP2 neurons (under the control of Scer\GAL4^eve.RN2 results in neuronal degeneration at very early stages of nervous system development (stage 13), strongly suggesting that manipulated aCC/RP2 neurons do not grow motor axons. The growth of the entire intersegmental motor nerve (ISN) is affected in approximately 26% of cases. Defects primarily consist of premature stalling of the nerve mostly at the level of muscles DO2/DA2. This indicates that, at rather low frequency, the nonmanipulated U and VUM neurons fail to reach their dorsal target muscles as a consequence of the absence of aCC/RP2.

Ablation of U neurons through the expression of Rcom\RA^Scer\UAS.cBa under the control of eve^{2xCQ.RC.T:Scer\GAL4} results in the U neurons being severely affected at early stage 13. Their ablation has an impact on the dorsal outgrowth of the intersegmental motor nerve in only 2.9% of cases.

Stage 16 Rcom\RA^Scer\UAS.cBa; Scer\GAL4^bs-23.26 embryos lack most ganglionic tracheal branches, but have normal glial populations and axonal tracts. The few ganglionic branch 1s that escape ablation migrate normally.

Targeted ablation of neurons using expression of Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^ftz.ng in embryos results in a reduction in mitosis in the longitudinal glia (LG) at the time when LG precursors normally divide upon neuronal contact, and an increase in division in the LG at later stages, when LG do not divide in wild-type embryos (assayed using pHis3 expression).

Flies expressing Rcom\RA^Scer\UAS.cSa under the control of Scer\GAL4^cad-em459 lack all terminal structures. The genital discs do not proliferate in third instar larvae.

Expression of Rcom\RA^Scer\UAS.cSa under the control of Scer\GAL4^how-24B results in a failure of germband retraction and the majority of the mesoderm often appears to be absent at 29^oC.

Expression of Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^C321c (resulting in the ablation of longitudinal glia) results in embryos in which 31% of ganglionic branches stall or turn to migrate posteriorly before they reach the longitudinal connectives. The formation of the longitudinal tracts is not detectably affected in these embryos. Expression of Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^Mz520 (resulting in the ablation of midline glia) results in 9% of ganglionic branches crossing the midline, while 5% linger along the midline or turn anteriorly. Some axons of the longitudinal tracts cross the midline in these embryos. Expression of Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^Mz820 results in embryos in which 6% of ganglionic branches turn to migrate posteriorly before crossing the longitudinal connectives while 8% of ganglionic branches linger around the midline.

Expression of Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^Dot.PK at 25^oC results in embryonic lethality. At 18^oC, adult flies expressing Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^Dot.PK are produced at 15% of the level expected. These flies have slightly rough eyes.

45% of embryos expressing Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^how-24B have excess cells at the dorsal midline of the embryonic brain and show thinning of the preoral brain commissure. The frontal commissure and ganglion are also absent.

Expression of Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^{GMR.in.Switch.PR} in animals exposed to RU486 results in disorganised eyes which are missing substantial numbers of ommatidia.

Some surviving adults expressing Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^PDM1 have rough eyes and very short and sparse bristles on the notum. Pharate adults expressing Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^A4 have small eyes. Adults expressing Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^{nAcRα-30D-P2} have roughness in the posterior part of the eye. Adults expressing Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^Eq1 have a longitudinal groove in the notum, a decrease in the number of bristles on the notum, malformed antennae, roughness at the eye equator and melanotic spots in the palpus.

Ablation of large numbers of embryonic CNS neurons using Rcom\RA^Scer\UAS.cBa; Scer\GAL4^ftz.ng leads to reduced numbers of longitudinal (interface) glial cells.

Rcom\RA^Scer\UAS.cBa driven by Scer\GAL4^30A is lethal at 25^oC. At 18^oC partial ablation of hemocytes are seen, without lethality. Newly eclosed flies open their wings fully, as per wild-type, though frequently dorsal and ventral surfaces of the wing are not bonded together. No melanotic tumours are seen. Many of the hemocytes that survive expression of Rcom\RA^Scer\UAS.cBa seem to be lamellocytes.

Neuronal ablation, caused by expression driven by Scer\GAL4^ftz.ng, leads to glial depletion caused by apoptosis. The remaining axons and glia cross the midline, within the commissures.

All macrophages are not eliminated in stage 13 embryos expressing Rcom\RA^Scer\UAS.cBa under the control of either Scer\GAL4^s.gcm or Scer\GAL4¹⁵⁸. Expression of Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^s.gcm results in the mosaic ablation of some glia in embryos (mosaic ablation can affect longitudinal glia in only one hemisegment) and loss of longitudinal axons in the central nervous system in 56% of hemisegments in stage 16 embryos. In extreme cases axonal depletion and fasciculation defects (the three fascicles collapse into one) are seen. The pioneer neurons MP1 and dMP2 are still present in hemisegments of the embryos in which glia have been ablated by expression of Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^s.gcm. The pioneer neurons vMP2, MP1 and dMP2 are still present in hemisegments of the embryos in which the interface glia have been ablated by expression of Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^s.gcm. In "severe" embryos in which many interface glia have been ablated by expression of Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^s.gcm the aCC, pCC and RP2 neurons are still present, although the aCC and pCC neurons may be slightly displaced. When longitudinal glia are ablated by expression of Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^s.gcm, the RP2 neuron is still present and is occasionally duplicated. Clusters of 2 to 4 apoptotic neuronal cells are seen in embryos after ablation of glia by expression of Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^s.gcm. These apoptotic cells are not seen in wild-type controls. Expression of Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4¹⁵⁸ results in the ablation of some glia in embryos and causes thinning of longitudinal tracts in the central nervous system. Neuronal apoptosis is induced in 40-42% of embryos in which interface glia have been ablated by expression of Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^C321c. A higher frequency of neuronal apoptosis than wild type is also seen in embryos in which glia have been ablated by expression of Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^s.gcm or Scer\GAL4¹⁵⁸.

When expression is driven by Scer\GAL4^c311, peripodial cells are ablated, the eye is reduced in size, consistent with a failure of furrow progression, and the surface of the shows severe patterning defects including square ommatidia.

Expression of Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^ato.3.6 results in the elimination of neurons in the brain that normally express ato. At 22^oC, only 18% of flies eclose compared to controls and at 28^oC no flies eclose. Escaper flies show a 2-3 day delay in eclosion compared to controls.

When the glioblast is ablated by the expression of Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^s.gcm, the dMP2 neuron extends more slowly than in wild-type embryos, as the axon is shorter than that in a normal adjacent segment or it does not meet the pCC/vMP2 fascicle and appears thickened and with a large growth cone. The dMP2 neuron does eventually extend and, slightly later, the growth cone may not branch out: the dMP2/MP1 axon heads towards the muscle fasciculating with the aCC neuron. Ablation of longitudinal glia by the expression of Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^s.gcm can lead to failure of contact and fasciculation between pCC/vMP2 and dMP2/MP1 fascicles at stage 13. Loss of the dMP2/MP1 pathway is often seen in stage 14 embryos, while the pCC/vMP2 fascicle is generally present. The pCC fascicle and aCC axons are thicker than normal at this stage, suggesting that the dMP2/MP1 fascicle fails to defasciculate from the pCC/vMP2 or aCC fascicles in the absence of glia. At stage 16, a single fascicle is seen instead of the two seen in wild-type embryos. The separation of the 3 longitudinal fascicles during stage 16 to 17 is damaged in 90% of segments. The 3 fascicles can appear fused into one single fascicle along the pCC pathway (in 41% of cases), fasciculation defects may affect only the second or third fascicles, fascicles can be missing or may misroute towards the muscle or midline. In the most extreme cases, the first fascicle is also damaged. Longitudinal follower axon tracts are missing, thin or broken, or misrouted towards the muscle or midline. Ablation of longitudinal glia by the expression of Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^s.gcm does not affect the pCC axon; no effect is observed when either the glia from its own segment or from the adjacent anterior segment is ablated. Ablation of glia and dMP2 and vMP2 neurons by the expression of Rcom\RA^Scer\UAS.cBa under the control of both Scer\GAL4^s.gcm and Scer\GAL4^15J2 causes a range of defects in the pCC neuron in 20% of cases including a dramatically enlarged growth cone, shorter or longer pCC axons, abnormally tortuous trajectory and fasciculation with the RP2 axon. The first fascicle has defasciculated, broken, misrouted or is missing in 42% of cases in stage 17 embryos.

The muscle pattern is extremely disrupted in embryos expressing Rcom\RA^Scer\UAS.cBa under the control of Scer\GAL4^nau.PM.

Longitudinal connectives are severely disrupted when expression is driven by Scer\GAL4^ftz.ng in the developing embryo: the follower neurons cannot establish the longitudinal pathways in the absence of pioneers. Axons are also misrouted across the midline. When expression is driven by Scer\GAL4^c544, Scer\GAL4^MZ465 or Scer\GAL4^15J2 axonal defects are evident at stage 14 but by stage 17 the pathways have recovered. When more than one set of pioneers are ablated by combining Scer\GAL4 driver inserts, the effect on pathfinding is increased in severity.

Scer\GAL4^sd-SG29.1-mediated expression for 1 hour at 37^oC causes cell death in the wing pouch.

Rcom\RT^A.UAS, Scer\GAL4^ftz.ng has embryonic longitudinal glial cell phenotype, suppressible by Df(3L)H99

Rcom\RT^A.UAS, Scer\GAL4^ftz.ng has embryonic longitudinal glial cell phenotype, suppressible | partially by Df(3L)H99

Rcom\RT^A.UAS, Scer\GAL4^s.gcm has embryonic/larval neuron phenotype, suppressible by BacA\p35^elav.PB