Males expressing Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^Gr32a.3.776 (to eliminate Gr32a-expressing gustatory receptor neurons) show reduced aggressive behavior (significantly increased latency to the first lunge and significantly reduced number of lunges) compared to wild type controls.

Males expressing Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^Gr32a.3.776 in the presence of Scer\GAL80^tsh-GAL80 (to eliminate Gr32a-expressing gustatory receptor neurons in the mouth only) show reduced aggressive behavior (significantly increased latency to the first lunge and significantly reduced number of lunges) compared to wild type controls. The mutant males show decreased male-male courtship compared to controls.

Expression of Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^{Orco.2.642.T:Hsim\VP22} from 2 hours after egg laying to 0-1 hours after pupariation formation (timing of expression controlled using the temperature sensitive Scer\GAL80^ts.αTub84B allele) results in the ablation of larval olfactory receptor neurons. DA1 and VA1d projection neuron dendrites show a marked ventromedial shift in these animals compared to wild type.

Males expressing Cbβ\DT-A^I.Scer\UAS under the control of one of Scer\GAL4^Gr32a.3.776, Scer\GAL4^Gr66a.PD or Scer\GAL4^Gr22e.PD show the same level of courtship towards decapitated females as do wild-type males.

Males expressing Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^Gr32a.3.776 show an increased courtship index towards decapitated males compared to the courtship index of wild-type males in this assay.

Males expressing Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^Gr66a.PD or Scer\GAL4^Gr22e.PD do not show an increased courtship index towards decapitated males.

Expression of Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^Or88a.cWa results in ablation of Or88a-expressing olfactory receptor neurons (ORNs), loss of presynaptic terminals and axons in the corresponding antennal glomerulus (VA1d), loss of its contralateral projections to the opposite antennal lobe, and a significant reduction in size of the corresponding glomerulus (VA1d). Or47b-expressing ORNs remain confined to the adjacent VA1lm glomerulus after ablation of Or88a-positive ORNs - they do not sprout as a result of nearby deafferented territories becoming available.

Expression of Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^Or47b.7.467 results in ablation of Or47b-expressing olfactory receptor neurons (ORNs) projecting to glomerulus VA1lm; Or88a-expressing ORNs remain confined to the adjacent VA1d glomerulus - they do not sprout as a result of nearby deafferented territories becoming available.

Induction of expression of Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^Mz19 upon eclosion leads to death of Scer\GAL4^Mz19-expressing projection neurons (PNs) 3 days later. 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.

Induction of expression of Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^GH146 upon eclosion leads to death of the majority of projection neurons (PNs). Nonetheless, the glomerular structures of the antennal lobe are essentially unaffected, and olfactory receptor neuron (ORN) axons projecting to the VA1d, VA1lm and DL1 glomeruli remain intact and do not expand to neighboring glomeruli.

Expression of Cbβ\DT-A^I.Scer\UAS under the simultaneous control of both Scer\GAL4^Or88a.cWa and Scer\GAL4^Mz19 results in the simultaneous ablation of Or88a-positive olfactory receptor neuron (ORNs) and projection neurons (PNs) projecting to the VA1d glomerulus. Nonetheless, the VA1d glomerulus is still readily distinguishable (by Mabnc82 staining) albeit significantly smaller - this size reduction is similar in magnitude to that caused by ablation of Or88a-expressing ORNs alone. The remaining glomerulus shows only a slight reduction of total presynaptic density compared to the control.

The electrophysiological response to water of a labellar I-type taste sensillum containing a single neuron marked by Scer\GAL4^NP1017 is disrupted when the marked neuron is killed or damaged by presense of Cbβ\DT-A^I.Scer\UAS. Responses of this sensillum to salt and sugar are unaffected. (Note, this genotype is pupal or larval lethal in whole animals, so this expriment was done by inducing somatic clones lacking Scer\GAL80^αTub84B.PL in a Cbβ\DT-A^I.Scer\UAS; Scer\GAL4^NP1017; Scer\GAL80^αTub84B.PL 'hsflp' background at 6 hours after puparium formation.)

Larvae that express Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^{Or83b.2.642.T:Hsim\VP22} (causing ablation of Or83b-expressing neurons) fail to respond to 17 out of 21 odours. Larvae which have ablated Or1a-expressing neurons (due to expression of Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^Or1a.PF) show reduced chemotaxis to (E)-2-hexenal but show normal chemotaxis to 19 other odours. Similarly, Scer\GAL4^Or49a.PF>Cbβ\DT-A^I.Scer\UAS larvae with ablated Or49a-expressing neurons show reduced chemotaxis to 1-hexanol only, while responses to other odorants are not affected. Scer\GAL4^Or42a.PF>Cbβ\DT-A^I.Scer\UAS larvae with ablated Or42a neurons show reduced chemotaxis to 4 out of 21 odours (octanol, isoamyl acetate, α-terpinene and ethylbenzene).

Ablation of pacemaker cells through expression of Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^P2.4.Pdf results in larvae that do not display photophobic behaviour. Increasing the light intensity to 1100 lux does not rescue photophobicity in Cbβ\DT-A^I.Scer\UAS Scer\GAL4^P2.4.Pdf larvae as they lack LNs.

When Cbβ\DT-A^I.Scer\UAS is driven by Scer\GAL4^npf.1 four neurons in the adult brain and the fan-shaped body are ablated. Mutant animals are significantly more resistant to the sedative effect of ethanol vapour, and recover from high doses of ethanol exposure more quickly than wild-type. These animals also show a slight increase in larval development and rate of egg-laying. These animals exhibit comparable ethanol levels when detected in their extracts. When Cbβ\DT-A^I.Scer\UAS is driven by Scer\GAL4^NPFR1.6.6 the mutant animals are significantly more resistant to the sedative effect of ethanol vapour, and recover from high doses of ethanol exposure more quickly than wild-type. These animals are more resistant than those expressing Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^npf.1. These animals also show no increase in larval development or rate of egg-laying.

Ablation of the ~30 sweet-sensitive gustatory neurons through expression of Cbbeta\DT-A^I.Scer\UAS under the control of Scer\GAL4^Tre.8.5.cCa does not affect the response to benzaldehyde.

Ablation of the ~25 bitter-sensitive gustatory neurons through expression of Cbbeta\DT-A^I.Scer\UAS under the control of Scer\GAL4^Gr66a.3.153 significantly reduces benzaldehyde avoidance. However, ablating bitter gustatory neurons does not decrease the BA avoidance of flies lacking olfactory organs.

When Cbβ\DT-A^I.Scer\UAS is driven by Scer\GAL4^Tre.8.5.cCa, mutant flies show reduced proboscis extension in response to sucrose, trehalose, glucose and low salt. These animals show a normal response to high salt. Mutants also show a normal response to berberine, caffein, denatonium and quinine. When Cbβ\DT-A^I.Scer\UAS is driven by Scer\GAL4^Gr66a.3.153, mutant flies show a normal response to sucrose, trehalose, glucose and low salt and high salt. Mutants are less sensitive to berberine, caffein, denatonium and quinine.

Larvae expressing Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^npf.1 show premature insensitivity in the feeding response; when young third

instar larvae are withheld from food for 2 hours and then transferred

to a solid glucose-agar disc placed on a large food-free agar plate,

only 5-12% of the mutant larvae remain on the glucose-agar disc after

20 minutes, in contrast to control larvae, where approximately 70%

remain on the glucose-agar disc after 20 minutes.

Larvae expressing Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^NPFR1.6.6

show premature insensitivity in the feeding response; when young third

instar larvae are withheld from food for 2 hours and then transferred

to a solid glucose-agar disc placed on a large food-free agar plate,

less than 20% of the mutant larvae remain on the glucose-agar disc

after 20 minutes, in contrast to control larvae, where approximately

70% remain on the glucose-agar disc after 20 minutes.

Larvae expressing Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^npf.1

which are withheld from food for 2 hours and then transferred to an

aliquot of yeast or 10% glucose paste placed on a large food-free agar

plate stay within the food and feed immediately (as do control larvae).

At the end of 20 minutes, 85-95% of both the control and mutant larvae

still remain inside the food.

Nearly all larvae expressing Cbβ\DT-A^I.Scer\UAS under the control

of Scer\GAL4^NPFR1.6.6 which are withheld from food for 2 hours

and then transferred to an aliquot of yeast or 10% glucose paste placed

on a large food-free agar plate remain inside the food after 20 minutes

(as do wild-type larvae).

Larvae expressing Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^npf.1

can discriminate between glucose-agar paste and water-agar paste in

a two-choice preference test.

Larvae expressing Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^npf.1

or Scer\GAL4^NPFR1.6.6 show an altered response compared to wild-type

larvae in a motivational feeding assay; young third instar larvae were

rinsed with water, withheld from food for 3 hours and then transferred

to a plate containing glucose-agar blocks. Many small cuts had been

made in the vertical surface of the agar blocks to accommodate one

larva per crack. Within 10 minutes, about 50% of the larvae had crawled

into a crack, which triggers feeding. Larvae expressing Cbβ\DT-A^I.Scer\UAS

under the control of Scer\GAL4^npf.1 or Scer\GAL4^NPFR1.6.6 had

a much lower frequency of mouth hook contractions than control larvae.

However, in an assay using liquid food (10% glucose-agar paste) the

mutant and control larvae have a similar, high frequency of mouth hook

contractions.

Third instar larvae expressing Cbβ\DT-A^I.Scer\UAS under the

control of Scer\GAL4^npf.1 or Scer\GAL4^NPFR1.6.6 show a shorter

average crawling distance on food-free agarose than control larvae,

but on glucose agarose the mutant larvae show a greater average crawling

distance than the control larvae.

Young third instar larvae expressing Cbβ\DT-A^I.Scer\UAS under

the control of Scer\GAL4^npf.1 or Scer\GAL4^NPFR1.6.6 which are

placed on a glucose-agar plate coated with a thin layer of yeast paste

tend to migrate to the periphery of the plate and form clumps of larvae

at the periphery when the plate is examined after 45 minutes. This

behaviour is typical of older wild-type third instar larvae, instead

of young wild-type third instar larvae which browse evenly across the

medium surface and do not show a tendency to aggregate.

Flies with Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^Switch2.30 (in the presence of RU486) die after 4-5 days. Flies with Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^Switch1.106 (in the presence of RU486) die after 5-6 days at 25^oC. At 18^oC they survive till day 7 but are female sterile. Survival of these flies is the same as wild-type in the absence of RU486). Cbβ\DT-A^I.Scer\UAS, (under the control of Scer\GAL4^Switch1.106 or Scer\GAL4^Switch2.30) flies after 3 days of RU486 treatment at 25^oC have completely ablated fat bodies.

Expression of Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^{tsl.T:Hsap\ESR1} (in the presence of β-estradiol or diethylstilbestrol to activate the Scer\GAL4^{tsl.T:Hsap\ESR1} protein) in adult females results in border cell and posterior polar follicle cell defects. 96% of stage 10 follicles lack border cells at the anterior edge of the oocyte, while the centripetal cells are unaffected. The posterior follicular epithelium appears discontinuous, suggesting that cells have died and been eliminated. Dead or dying cells are present at the two poles of the follicle. The posterior "polar pair" follicle cells appear intact, even in follicles with obvious disruption to the posterior follicular epithelium. The anterior "polar pair" follicle cells are morphologically normal, but fail to migrate to the edge of the oocyte. Oocyte polarity is unaffected. The distinctive cell imprints that form the aeropyle are reduced in number or completely absent in eggs derived from females expressing Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^{tsl.T:Hsap\ESR1} (in the presence of β-estradiol or diethylstilbestrol to activate the Scer\GAL4^{tsl.T:Hsap\ESR1} protein) and the micropyle appears to be blocked. 92% of the eggs laid between 60-84 hours of hormone treatment are unfertilised. Expression of Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^{tsl.T:Hsap\ESR1} (in the presence of β-estradiol or diethylstilbestrol to activate the Scer\GAL4^{tsl.T:Hsap\ESR1} protein) during the larval stage results in lethality; very few larvae pupate and none eclose. Expression of Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^ER212, Scer\GAL4^ER168, Scer\GAL4^ER156, Scer\GAL4^ER115 or Scer\GAL4^ER54 during larval stages (in the presence of β-estradiol to activate the Scer\GAL4 protein) results in lethality. Expression of Cbβ\DT-A^I.Scer\UAS under the control of Scer\GAL4^ER168 (in the presence of β-estradiol or diethylstilbestrol to activate the Scer\GAL4^ER168 protein) in females results in alterations in oocyte polarity.