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General Information
Symbol
Dmel\dnc1
Species
D. melanogaster
Name
dunce1
FlyBase ID
FBal0002713
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dunce1
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
Expression Data
Reporter Expression
No Assay Recorded
Stage
Tissue/Position (including subcellular localization)
Reference
immunolocalization
Stage
Tissue/Position (including subcellular localization)
Reference
Additional Information
Statement
Reference
Immunolocalization of dnc protein to thin sections of adult brain shows that it is largely concentrated in the mushroom bodies. Within mushroom bodies, the γ lobes stain more intensely than the α or β lobes, peduncle staining intensity varies with position and calyx expression is uniform. An intermediate level of staining is seen in most neuropil structures including the inner optic lobe neuropil, protocerebrum, suboesophageal ganglion, antennal lobes, and central complex. A conspicuous lack of staining is found in the photoreceptor cell layer, lamina, antennal nerve, and median bundle. The pattern of dnc1 protein was indistinguishable in heads from the wild type pattern.
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 1 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference
dnc1 adult homozygotes do not display any overt eye morphology defects but display memory defects in an aversive olfactory conditioning assay (their olfactory perception however is not disrupted).
dnc1 hemizygous males display a significant decrease in intermediate-term (3h after conditioning) olfactory memory, which is more severe if individuals are subjected to cold-shock anesthesia after conditioning, as compared to controls.
Upon initial exposition, dnc1 adult mutants show ethanol sensitivity that is comparable to wild-type controls but exhibit reduced development of tolerance (= increase in resistance during re-exposition).
dnc1 homozygous adults show significant decrease in the amnestic cooling resistant memory component at 3 hr post-training in an olfactory memory assay compared to controls.
dnc1 mutant adult males do not display any immediate recall memory (assayed immediately after training) or short-term memory (60 min after training) in the courtship behavior experimental paradigm (the male is paired with an unreceptive female during training and than paired with either receptive virgin female or unreceptive pre-mated females for the memory experiments).
Homozygous dnc1, dnc1/dncM14 and dnc1/dncML adults show a significant reduction in performance index in an aversive olfactory learning assay compared to control flies.
dnc1 mutant third instar larvae exhibit learning defects in odor-association learning assays.
dnc1 mutant larvae have a significantly reduced ability to form aversive associative olfactory memories in response to high salt concentration compared to wild-type controls.
Homozygous males show a defect in courtship conditioning: the courtship index of homozygous males that have previously courted non-receptive females is not significantly reduced compared to males that have not undergone conditioning (in contrast to wild-type males, where conditioned males show a reduced courtship index compared to unconditioned controls).
Mutant males lack 30-minute courtship memory after 1 hour of conditioning in a courtship conditioning assay.
59.1% of mutant flies are rhythmic for locomotor activity under constant darkness conditions.
Mutant flies show an increased arousal threshold (the minimal vibration required to arouse a quiescent fly) compared to controls.
dnc1 heterozygotes exhibit a reduction in olfactory learning and long term memory in a negatively reinforced olfactory learning paradigm.
dnc1/dnc1 mutant flies exhibit defective short term memory (3 min after odor training), defective midterm memory, and defective anaethesia-resistant memory, but not defective anaesthesia-sensitive memory, when cold-amnestic treatment is applied 30 min before testing 3 h odor memory, as compared to controls.
Compared with wild-type, dnc1 mutants display an increase in varicosity number normalised to muscle surface area.
dnc1/Y males show a defect in 2 hour memory compared to wild type.
Aversive memory fails to form after associative linalool/quinine hemisulfate conditioning in dnc1 mutant larvae.
Expression of dncScer\UAS.cCa using Scer\GAL4osk-norka in a dnc1 background results in lethality at the larval stage.
Homozygous dnc1 mutant flies show decreased avoidance of high temperatures. dnc1/dncM14 mutant flies show decreased avoidance of high temperatures.
dnc1 mutants live significantly longer than controls.
Homozygous dnc1 mutants exhibit normal spontaneous odor identity discrimination. Homozygous dnc1 mutants exhibit disrupted conditioned odor identity discrimination.
In contrast to wild-type, dnc1 mutants do not reveal specificity in the 20-30Hz frequency range for attention-span clumping. In dnc1 mutants, the frequency domain for attention responses seems lower than in wild-type.
Mutant flies show attenuated and delayed brain responses (assayed by measuring local field potential activity in the brain) to a visual object moving around the fly once every 3 seconds, as compared to wild-type flies. Mutant flies fail to show any selective 20- to 30Hz response to a novel visual stimulus after a transition (in contrast to wild-type flies), and instead show some selective responsiveness in the 10- to 2-Hz range. Mutant flies show a strong optomotor response in an optomotor paradigm assay. However, the mutant flies show a delayed optomotor response when progressing through a maze, proceeding through the first two choice points without displaying any optomotor response but then responding strongly (showing a preference for turning into the direction of perceived motion) at the remaining choice points. Mutant animals are not distracted by a competing visual stimulus added to an optomotor assay, in contrast to wild-type flies.
Waking experience has no impact on subsequent sleep need in dnc1 homozygotes, in contrast to control flies.
Mutant males fail to show trainer-specific suppression of courtship, decreasing courtship toward a mature virgin after training with either mature or immature females. the ability to discriminate between mated and virgin females remain intact.
dnc1 mutant larvae, trained with LIN/SUC fail to exhibit a Response Index (RI) increase, unlike wild-type flies.
Unlike wild-type males, dnc1 homozygous males that have undergone courtship conditioning (kept in the presence of a female for 7 hours) do not spend significantly less time engaged in courtship behaviour when placed with a female 5 days after conditioning than non-conditioned males of the same genotype.
Mutants exhibit a synaptic over-growth phenotype.
dnc1 and dnc1/dncM11 larval motor nerve termini show decreased levels of varicosity and branch numbers compared to wild type, when larvae are raised at either room temperature or 30oC.
The average amplitudes of synaptic currents recorded in dnc1 mutant aCC and RP2 motorneurons are significantly larger than in wild type and the resting potential of these neurons is depolarized relative to wild type. However, the frequency of synaptic currents is not significantly different. The ability of aCC/RP2 to fire action potentials in response to an injection of constant current is decreased in dnc1 mutants compared to wild type.
The volume of the antennal lobe and of individual DM2, V and DM6 glomeruli in 6 day old adults is not altered compared to wild type.
Injection of serotonin or norepinephrine increases the heart rate in dnc1 mutant pupae, and the change in rate is no different from that seen in wild-type controls.
In wild-type flies, long-term exposure to concentrated odorants can lead to induced adaptation of certain olfactory glomeruli. Homozygous dnc1 mutants do not show this adaptation.
The electroantennogram (EAG) of mutant flies shows a slowed voltage change in response to ethyl acetate, with the correspondent rise time (RT) value becoming significantly different from wild type at the highest concentration of ethyl acetate used. Onset kinetics for acetone EAGS show slower kinetics compared to wild type. In response to benzaldehyde, the EAG rising phase is slower than normal in mutant flies and RT differences compared to wild type appear very close to statistical signification. At high concentrations of odorant, mutant flies are less sensitive to ethyl acetate than control flies in a behavioural assay. Sensitivity to acetone is reduced. Sensitivity to benzaldehyde is increased.
While the learning index in wild-type flies persists for at least eight hours at the level reached immediately after completion of training, the learning index in dnc1 mutants is significantly lower than it is in the wild-type by one hour after training. By three hours after training, the learning index in dnc1 mutants is not different from zero.
During 30 Hz stimulation of the neuromuscular junction, mobilisation and translocation of vesicles from the reserve pool (RP) to the exo/endo cycling pool (ECP) is enhanced in dnc1, resulting in a smaller RP. Bafilomycin treated preparations from dnc1 mutants stimulated at 1Hz for a prolonged period of time led to markedly decreased amplitude of evoked potentials, as seen in wild-type. Subsequent stimulation at 10Hz for 10s increased the amplitude in dnc1, as in wild-type, but instead of the amplitude increasing gradually and then being maintained for some time after the cessation of stimulation, as seen in wild-type, the amplitude increased and decreased rapidly in response to the change in stimulation.
The incidence of cholinergic spontaneous excitatory postsynaptic currents (sEPSCs) in dnc1 neurons in culture is not different to the incidence rate seen in wild-type neurons in culture. The mean sEPSC frequency in dnc1 neurons is significantly higher than in wild-type neurons. The average miniature EPSC (mEPSC) frequency in dnc1 neurons is significantly higher than in wild-type neurons. The amplitude and kinetic properties of the mEPSCs are similar to wild type. A persistent increase in mEPSC frequency is induced by repetitive, spaced db-cAMP exposure in wild-type neurons in culture, but is absent in dnc1 neurons in culture.
Acetylcholine currents are reduced in peak amplitude in cultured dnc1 "giant" neurons. There are events with markedly slower kinetics of rise and decay compared to wild-type neurons. The frequency of spontaneous ACh release in these neurons is similar to wild type.
Approximately 30% of neurons from homozygous larval brains display a cAMP-sensitive outward current. This is a significant reduction compared to wild-type. Only 5% of homozygous mushroom body neurons have outward currents that are down-modulated by cAMP. This is a significant reduction compared to the neuron population of homozygous larval brains as a whole. Neurons with an outward current dominated by a rapidly inactivating outward current and not modulated by cAMP are more abundant in homozygous larval brains compared to wild-type.
Flies show reduced learning and memory compared to wild-type. The flies have abnormal nonassociative abilities.
Hemizygous males show a slightly increased sensitivity to ethanol in an inebriometer assay.
After presentation of electric shock with a first odour, dnc1 flies show a strongly reduced avoidance of a second, different odour compared to wild-type flies.
dnc1 flies kept in constant darkness have a smaller lamina volume than dnc1 flies kept in constant light, as is also seen for wild-type flies.
Growth cone exploratory movement is nearly arrested. Phenotype can be mimicked by normal neurons when perfused with db-cAMP (dibutyryl cAMP) or forskolin. Motility is also restored by counterbalancing the effects in rut dnc double mutants.
Flies have a low learning score in an olfactory classical conditioning paradigm.
The delay portion and point of maximal phase delay of the light induced phase response curve (PRC) differs significantly from that of wild type and the circadian period is significantly shorter.
Homozygous larvae show no initial learning in an odour avoidance test. Homozygous adults derived from larvae conditioned using the odour avoidance test show no memory retention, in contrast to wild-type flies.
Flies transformed with the P{dnchs.P} or P{rat\dnchs.P} construct display increased learning scores.
Reduced grooming activity.
The voltage-activated transient K+ current (IA) in the larval muscle fibres of both heterozygotes and homozygotes is increased compared to wild-type. The voltage-activated delayed K+ current (IK) in the larval muscle fibres of homozygotes is increased compared to wild-type, but is almost normal in the larval muscle fibres of heterozygotes.
Mutants exhibit enhanced motor terminal aborization, this suggests cAMP levels influence the size of motor axon projections. Introduction of rut1 counterbalances this effect.
The sensory neuron innervating the antero-notopleural bristle has an abnormally large number of side branches and varicosities in a defined segment of the axon. Ultrastructure studies suggest that the varicosities are potential synaptic sites.
The anteronotopleural neuron responds to deflection of the bristle with a burst of action potentials, and shows adaptation in response to a sustained deflection towards the body wall. The sensory response to repetitive stimulation is independent of CNS feedback. The anteronotopleural neuron fatigues more than that of wild type.
Sensitisation to sucrose wanes unusually rapidly in mutant flies.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
dnc1 has female sterile phenotype, enhanceable by cff1
Suppressed by
Statement
Reference
Enhancer of
Statement
Reference
Suppressor of
NOT Suppressor of
Statement
Reference
dnc1 is a non-suppressor of locomotor rhythm defective phenotype of Nf1P2
dnc1 is a non-suppressor of locomotor rhythm defective phenotype of Nf1P1
Other
Statement
Reference
Phenotype Manifest In
Enhanced by
Statement
Reference
dnc1 has phenotype, enhanceable by cff1
Suppressed by
Statement
Reference
dnc1 has synapse | ectopic phenotype, suppressible by GαsB19
dnc1 has phenotype, suppressible by rut1
Additional Comments
Genetic Interactions
Statement
Reference
Adult males that are both hemizygous for dnc1 and homozygous for Rgk1Δ exhibit a severe decrease in cold-shock anesthesia-resistant intermediate-term olfactory memory (3h after conditioning) as compared to adult males that are only hemizygous for dnc1 or only homozygous for Rgk1Δ.
The short-term memory defects (assayed in the courtship behavior experimental paradigm) observed in either Fmr1FS or dnc1 single mutant adult males are restored in the double mutants.
DopEcRc02142 restores 30-minute courtship memory in a courtship conditioning assay in dnc1 males.
Locomotor activity behaviour under 12 hour light/12 hour dark conditions is partially rescued in flies expressing gwHMS00105 under the control of Scer\GAL4tim.PE (in the presence of Dcr-2Scer\UAS.cDa) if they are also mutant for dnc1. The evening peak phase is rescued closer to a wild type value, while the morning peak is not restored. 41.0% of flies expressing gwHMS00105 under the control of Scer\GAL4tim.PE (in the presence of Dcr-2Scer\UAS.cDa) in a dnc1 background are rhythmic for locomotor activity under constant darkness conditions.
Trans-heterozygotes of Fmr13 and dnc1 do not exhibit learning or long term memory deficits.
dnc1/dnc1, rut1/rut1 double mutants exhibit an even greater decrease in performance index in short term memory, as compared to either single mutant, and there is no significant difference in perception of task relevant stimuli (odors and electric shock), as compared to controls.
The lifespan of dnc1; Nf1P2 flies is as wild-type, indicating that the reduced life span found in Nf1P2 mutants is the product of reduced cAMP levels.
The addition of G-sα60AB19 suppresses the synaptic over-growth phenotype seen in dnc1 mutants.
Rat\RD1hs.PD partially rescues the low learning score phenotype in the absence of heat shock, and the rescue is increased after heat shock.
Double mutants with stnA7 die within the pupal case or shortly after emergence, due to uncoordination. Double mutants with stnA15 show no greater debilitation or stress sensitivity than stnA15. Double mutants with stnA15 show no greater debilitation or stress sensitivity than stnA15. dnc1, parats1 and dnc1, shi1 double mutants show no more severe effect than either paralytic mutant alone. Su(stn)1 suppresses the lethal interaction of dnc1, stnA7.
The effects of Sh and eag mutants can be potentiated by mutations in dnc and the enhancement can be counterbalanced by rut1. The effect of extreme hyperexcitability in eag Sh double mutants cannot be potentiated by mutations in dnc.
Xenogenetic Interactions
Statement
Reference
dnc1 suppresses the locomotor defects in flies induced by Scer\GAL4elav-C155-driven overexpression of Hsap\APPAβ1-42.Scer\UAS.cIa.
Complementation and Rescue Data
Rescued by
Comments
Expression of dncScer\UAS.cCa under the control of Scer\GAL4elav.PU rescues the defective short term memory performance of dnc1/dnc1 mutants, whether expressed throughout development or with expression restricted to adult stage with the use of a Gal80[ts] transgene. Expression of dncScer\UAS.cCa under the control of both Scer\GAL4GH298 and Scer\GAL4ey-OK107, both Scer\GAL4GH298 and Scer\GAL417d, both Scer\GAL4GH298 and Scer\GAL4NP1131, both Scer\GAL4GH298 and Scer\GAL4c320, both Scer\GAL4GH298 and Scer\GAL4c305a, both Scer\GAL4GH298 and Scer\GAL4Mef2.247, or both Scer\GAL4NP1227 and Scer\GAL4Mef2.247 (but not under the control of any one of Scer\GAL4GH298, Scer\GAL4NP1227, Scer\GAL4Orco.PU, Scer\GAL4Mef2.247, or Scer\GAL4NP0225 alone) rescues the defective short term memory performance of dnc1/dnc1 mutants. Expression of dncScer\UAS.cCa under the control of both Scer\GAL4GH298 and Scer\GAL417d, both Scer\GAL4GH298 and Scer\GAL4NP1131, both Scer\GAL4GH298 and Scer\GAL4c305a, or both Scer\GAL4GH298 and Scer\GAL4Mef2.247 (but not under the control of one of Scer\GAL4Mef2.247 or Scer\GAL4GH298 alone) rescues the defective anaesthesia-resistant memory performance of dnc1/dnc1 mutants.
Expression of dncScer\UAS.cCa using Scer\GAL4rafl-1 or Scer\GAL4c309 rescues the aberrant brain responses to novelty seen in dnc1 flies. Use of Scer\GAL4val-1 results in partial rescue of this phenotype. Expression of dncScer\UAS.cCa using Scer\GAL4toi-1 does not rescue the aberrant brain responses to novelty seen in dnc1 flies. Expression of dncScer\UAS.cCa using Scer\GAL4c309, but not Scer\GAL4val-1 or Scer\GAL4toi-1, rescues the defective optomotor behaviour of dnc1 flies.
The low learning score phenotype is partially rescued by dnchs.PD expressed using heat shock.
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Byers.
Comments
Comments
Enzyme activity is 51% of wild-type.
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (86)