FlyBase Allele Report: Dmel\Adcy1[rut-1]

General Information

Symbol

Dmel\Adcy1^rut-1

Species

D. melanogaster

Name

FlyBase ID

FBal0014878

Feature type

allele

Associated gene

Dmel\Adcy1

Associated Insertion(s)

Carried in Construct

Also Known As

rut¹, rutabaga¹

Key Links

Allele class

loss of function allele

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

loss of function allele

(Zhong and Wu, 2004)

Mutagen

ethyl methanesulfonate

(Feany, 1990)

Progenitor genotype

Cytology

Description

Single point mutation substituting adenine for guanine at position 3459, corresponding to arginine substituted for glycine at amino acid 1026.

(Levin et al., 1992)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

Expression Data

Reporter Expression

Additional Information

Statement

Reference

Marker for

Reflects expression of

Reporter construct used in assay

Human Disease Associations

Disease Ontology (DO) Annotations

Models Based on Experimental Evidence ( 1 )

Disease

Evidence

References

model of alcohol use disorder

CEA

(Moore et al., 1998)

Modifiers Based on Experimental Evidence ( 1 )

Disease

Interaction

References

exacerbates Parkinson's disease

modeled by Hsap\APP^{Aβ42.UAS.Tag:SS(rPENK)}

(Iijima-Ando et al., 2009)

exacerbates neurofibromatosis

modeled by Nf1^P2

(Tong et al., 2007)

ameliorates epilepsy

modeled by para^bss1

(Saras and Tanouye, 2016)

modeled by eas²

(Saras and Tanouye, 2016)

modeled by jus^iso7.8

(Saras and Tanouye, 2016)

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal behavior | recessive

(Phillis et al., 1993)

abnormal learning

(Honjo and Furukubo-Tokunaga, 2009, Liu et al., 2009, Guo et al., 2000)

abnormal memory

(Qin and Dubnau, 2010, Tan et al., 2010, Blum et al., 2009, Honjo and Furukubo-Tokunaga, 2009, Honjo and Furukubo-Tokunaga, 2005)

abnormal memory (with Adcy1^rut-2080)

(Blum et al., 2009)

abnormal memory | adult stage

(Scholz-Kornehl and Schwärzel, 2016, Scheunemann et al., 2012)

abnormal neuroanatomy

(Renger et al., 2000, Shayan and Atwood, 2000)

abnormal neuroanatomy | larval stage

(Bhattacharya et al., 1999)

abnormal neuroanatomy | third instar larval stage

(Chen and Ganetzky, 2012, Guan et al., 2011)

abnormal neurophysiology

(Hou et al., 2003, Martin et al., 2001, Kuromi and Kidokoro, 2000, Renger et al., 2000)

abnormal neurophysiology | dominant | larval stage

(Kim et al., 2024)

abnormal neurophysiology | larval stage

(Bhattacharya et al., 1999)

abnormal sleep

(Hendricks et al., 2001)

abnormal smell perception

(Xia and Tully, 2007, Honjo and Furukubo-Tokunaga, 2005, Martin et al., 2001)

abnormal taste perception

(Honjo and Furukubo-Tokunaga, 2005)

abnormal thermotaxis

(Hong et al., 2008)

chemical sensitive

(Moore et al., 1998)

decreased efficacy of learning | adult stage

(Tener et al., 2024)

decreased efficacy of memory | adult stage

(Tener et al., 2024)

Phenotype Manifest In

axon & motor neuron | conditional ts

(Zhong and Wu, 2004)

axon | third instar larval stage

(Guan et al., 2011)

calyx of adult mushroom body

(Hitier et al., 1998)

dense body

(Shayan and Atwood, 2000)

embryonic/larval neuromuscular junction | larval stage

(Kim et al., 2024)

embryonic/larval neuromuscular junction | third instar larval stage

(Chen and Ganetzky, 2012)

neuromuscular junction

(Kuromi and Kidokoro, 2000, Renger et al., 2000, Shayan and Atwood, 2000)

neuromuscular junction & abdominal 4 ventral longitudinal muscle 3 & larva

(Cheung et al., 1999)

neuromuscular junction & abdominal 4 ventral longitudinal muscle 4 & larva

(Cheung et al., 1999)

neuromuscular junction | larval stage

(Cheung et al., 1999)

neuromuscular junction | third instar larval stage

(Guan et al., 2011)

NMJ bouton | third instar larval stage

(Chen and Ganetzky, 2012)

RP3 neuron & synapse

(Renger et al., 2000)

RP3 neuron & synaptic vesicle

(Renger et al., 2000)

synapse

(Renger et al., 2000, Shayan and Atwood, 2000)

varicosity | third instar larval stage

(Guan et al., 2011)

Detailed Description

Statement

Reference

rut¹ homozygous mutant adults have a similar increase in aversive olfactory 24 h memory observed when the recall environment better matches the training environment (presence of copper grid) to controls.

(Zhao et al., 2019)

rut¹ homozygous adults show significant decrease in the amnestic cooling sensitive memory component at 3 hr post-training in an olfactory memory assay compared to controls.

(Scholz-Kornehl and Schwärzel, 2016)

rut¹ causes a mild neuromuscular junction (NMJ) undergrowth phenotype. Heterozygous rut¹ larvae have NMJs that do not differ from wild-type.

(Chen and Ganetzky, 2012)

rut¹/rut¹ mutant flies exhibit defective short term memory (3 min after odor training), defective midterm memory, and defective anaethesia-sensitive memory, but not defective anaesthesia-resistant memory, when cold-amnestic treatment is applied 30 min before testing 3 h odor memory, as compared to controls.

(Scheunemann et al., 2012)

Compared with wild-type, rut¹ mutants show a decrease in synaptic varicosity number when normalised to muscle surface area. In addition , they display a decrease in axonal branch number and innervation length.

(Guan et al., 2011)

rut¹ mutants do not display any changes in synaptic morphology compared to wild-type.

(Lee and Wu, 2010)

rut¹ mutants exhibit approximately 50% of the normal memory performance of wild-type controls, both immediately after a training session and 24 hours after spaced training. Extinction learning appears to be normal in these mutants. With either 10 or 30 sessions of extinction there is a significant inhibitory extinction in these mutants.

(Qin and Dubnau, 2010)

Mutants show a significant impairment in 3 minute memory after olfactory conditioning compared to wild-type flies.

(Tan et al., 2010)

Homozygous and rut¹/rut²⁰⁸⁰ adults show severely reduced 2 minute memory after a single aversive Pavlovian training session. These adults also show severely reduced memory performance 24 hours after either ten massed or ten spaced sessions of training.

(Blum et al., 2009)

Aversive memory fails to form after associative linalool/quinine hemisulfate conditioning in rut¹ mutant larvae.

(Honjo and Furukubo-Tokunaga, 2009)

rut¹ flies show significantly lower learning after aversive olfactory conditioning (flies trained to associate odors with an electric shock) or after appetitive olfactory conditioning (with 1.0M sucrose presented with a conditioned odor), compared to controls.

(Liu et al., 2009)

rut¹ mutant flies show decreased avoidance of low temperatures.

(Hong et al., 2008)

rut¹ mutants exhibit significantly shorter life spans compared to controls.

rut¹ flies exhibit a delay in recovery time from a 20 minute 37[o]C heat stress, as shown by a locomotive index generated with a climbing assay.

Mitochondrial aconitase activities in 30-day old rut¹ flies are reduced by 75% compared to controls.

Superoxide levels are increased in rut¹ flies compared to controls.

(Tong et al., 2007)

Homozygous rut¹ mutants exhibit normal spontaneous odor identity discrimination.

Homozygous rut¹ mutants exhibit disrupted conditioned odor identity discrimination.

(Xia and Tully, 2007)

rut¹ mutant larvae, trained with LIN/SUC, LIN with DW, or SUC alone fail to exhibit a Response Index (RI) increase, unlike wild-type flies. The gustatory response for SUC is slightly lower in rut¹ larvae than in wild-type flies.

(Honjo and Furukubo-Tokunaga, 2005)

Mutant larvae show no significant defects in synapse formation.

(Wolfgang et al., 2004)

When raised at room temperature or at 25^oC, the motor axon terminals of rut¹ larvae show a similar level of arborization to wild-type larvae. However, the motor nerve termini of wild-type larvae raised at 30^oC show greatly increased levels of branching and variscosities, while no such large increase in terminal projection.

(Zhong and Wu, 2004)

Facilitation during tetanus is slightly reduced and post-tetanic potentiation is lacking in rut¹ embryos. The frequency and amplitude of miniature synaptic currents (mSCs) is not significantly different from controls. However, in saline with high K⁺ the frequency of mSCs is lower than in controls.

(Hou et al., 2003)

Injection of serotonin or norepinephrine increases the heart rate in rut¹ mutant pupae, and the change in rate is no different from that seen in wild-type controls.

(Johnson et al., 2002)

Mutant flies show a significant increase in the number of rest hours per 24 hours compared to controls.

(Hendricks et al., 2001)

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. 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.

(Martin et al., 2001)

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 depressed in rut¹, resulting in a larger RP. Bafilomycin treated preparations from rut¹ 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 does not increase the amplitude in rut¹, as compares to wild-type. However,, asn increase in the amplitude of evoked potentials is observed during and after the second or third application of 10Hz stimulation. Furthermore, when rut¹ mutants which were pre-treated with bafilomycin and stimulated at 1Hz, is incubated with 300μM db-cAMP for 25 minutes, the amplitude of potentials evoked at 1Hz is not affected or slightly increased. However, the amplitude of potentials evoked at 10Hz for 10s gradually increases during stimulation, and the increase continues for about 30 s, as observed in wild-type.

(Kuromi and Kidokoro, 2000)

The number of synapses per unit length of terminal is reduced greater than twofold compared to controls in both axons 1 and 2 (from neurons RP3 and 6/7b respectively) at the neuromuscular junction of muscles 6 and 7 of third instar rut¹/Y larvae. Synapses of axon 1 are approximately threefold larger than controls and axon 2 terminals also show an increase in synapse size. The number of active-zone dense bars is increased compared to controls. A much greater variability in synapse area is seen compared to controls. The ratio of docked to undocked vesicles is lower than in wild type in axon 1 synapses. The frequency of spontaneous release (miniature excitatory junctional currents - mejcs) at the neuromuscular junction is reduced compared to wild type. There is a Ca²⁺-independent increase in the decay time of mejcs. Evoked ejcs show a high frequency of failures and reduced release. There is a significant reduction in the mean quantal content. The peak amplitude of evoked ejcs is consistently lower than in wild type. Broadened or multiple peaks occur in evoked ejcs. There is increased variability in the time to peak of evoked ejcs. There is a Ca²⁺-dependent increase in the decay time of evoked ejcs. Boutons show altered short-term plasticity.

(Renger et al., 2000)

The mean synaptic area for synapses in individual type Ib and Is varicosities is significantly increased in rut¹ animals compared to controls. The number of dense bodies per synapse is modestly increased in type Ib but not in type Is varicosities.

(Shayan and Atwood, 2000)

The peak dihydropyridine (DHP)-sensitive current in rut¹ larval muscles cannot be increased by application of 1μm forskolin.

(Bhattacharya et al., 1999)

rut¹ larvae have fewer type Ib and type Is varicosities at the neuromuscular junction of muscles 6 and 7 of abdominal segment 4 compared to wild type. There is a reduction in excitatory junction potential (EJP) amplitude at muscles 6 and 7 compared to wild type.

(Cheung et al., 1999)

rut¹ flies have calyxes that are reduced in volume by 2.8% compared to control flies. In wild-type animals, increasing the density at which larvae are reared results in an increase in the volume of the calyx in the adult brain. This plasticity is still seen in rut¹ mutants.

(Hitier et al., 1998)

Hemizygous males show increased sensitivity to ethanol in an inebriometer assay. The ethanol-sensitive phenotype is reversed by treatment of the flies with forskolin (an adenylate cyclase activator).

(Moore et al., 1998)

After presentation of electric shock with a first odour, rut¹ flies show a strongly reduced avoidance of a second, different odour compared to wild-type flies.

(Preat, 1998)

rut¹ flies kept in constant darkness have a smaller lamina volume than rut¹ flies kept in constant light, as is also seen for wild-type flies.

(Barth et al., 1997)

Modulation of voltage gated K⁺ currents induced by the neuropeptide pituitary adenylyl cyclase-activating polypeptide (PACAP38) is eliminated. Application of cAMP analogs or forskolin is sufficient to restore PACAP38 enhancement of K⁺ currents.

(Guo et al., 1997)

Mutant diminishes cAMP synthesis and reduced the rate of habituation (using the jump-and-flight escape response). Habituation is extremely rapid in dnc rut double mutants.

(Engel and Wu, 1996)

Growth cone exploratory movement is nearly arrested. Growth cones become active when perfused with db-cAMP (dibutyryl cAMP). Motility is also restored by counterbalancing the effects in rut dnc double mutants.

(Kim and Wu, 1996)

Slightly reduced grooming behavior.

(Phillis et al., 1993)

The voltage-activated transient K⁺ current (I_A) in the larval muscle fibres of homozygotes is normal. The voltage-activated delayed K⁺ current (I_K) in the larval muscle fibres of homozygotes is almost normal. The amplitude of the delayed plateau outward K⁺ current (I_S) in the larval muscle fibres of rut¹ animals is reduced to levels below that of wild-type if the fibres are treated with caffeine.

(Zhong and Wu, 1993)

Mutation abolished catalytic activity.

(Levin et al., 1992)

Reduction in basal level of adult adenylate cyclase. Calcium insensitive.

(Whitehouse-Hills et al., 1992)

Lack of PTP and reduced facilitation.

(Zhong and Wu, 1991)

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 less than that of wild type.

(Corfas and Dudai, 1990)

Sex-dependent enhancement in pertussis toxin catalysed ADP-ribosylation with respect to wild type: attributed in part to an increase in the α subunit of the G₀-like protein.

(Guillen et al., 1990)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Adcy1^rut-1 has abnormal memory | adult stage phenotype, enhanceable by Pde4^dnc-1/Pde4^dnc-1

(Scheunemann et al., 2012)

Adcy1^rut-1 has abnormal memory phenotype, enhanceable by Nmdar1^EP331

(Qin and Dubnau, 2010)

NOT suppressed by

Statement

Reference

Adcy1^rut-1 has abnormal learning phenotype, non-suppressible by Scer\GAL4^c747/Rdl^RNAi.2-7.UAS

(Liu et al., 2009)

Adcy1^rut-1 has abnormal learning phenotype, non-suppressible by Scer\GAL4^c747/Rdl^RNAi.4-5.UAS

(Liu et al., 2009)

Enhancer of

Statement

Reference

Adcy1^rut-1/Adcy1^rut-1 is an enhancer of abnormal memory | adult stage phenotype of Pde4^dnc-1

(Scheunemann et al., 2012)

rut[+]/Adcy1^rut-1 is an enhancer of abnormal memory phenotype of Nmdar1^EP331

(Qin and Dubnau, 2010)

Adcy1^rut-1 is an enhancer of abnormal locomotor behavior phenotype of Hsap\APP^{Aβ42.UAS.Tag:SS(rPENK)}, Scer\GAL4^ChAT.7.4

(Iijima-Ando et al., 2009)

NOT Enhancer of

Statement

Reference

Adcy1^rut-1 is a non-enhancer of abnormal locomotor behavior | adult stage | conditional phenotype of Cnoc\ChR1::Csub\ChR^{CsChrimson.IVS.20xUAS.Venus}, Scer\GAL4^0273-G4

(Stern et al., 2019)

Adcy1^rut-1 is a non-enhancer of abnormal neuroanatomy | larval stage phenotype of Fak^K24/Fak^N30

(Tsai et al., 2012)

Suppressor of

Statement

Reference

Adcy1^rut-1 is a suppressor | partially of abnormal neuroanatomy | dominant | third instar larval stage phenotype of Lapsyn^zg1

(Guan et al., 2011)

Adcy1^rut-1 is a suppressor of abnormal neuroanatomy phenotype of slo¹

(Lee and Wu, 2010)

Adcy1^rut-1 is a suppressor of abnormal neuroanatomy phenotype of sei²

(Lee and Wu, 2010)

NOT Suppressor of

Statement

Reference

Adcy1^rut-1 is a non-suppressor of abnormal locomotor behavior | adult stage | conditional phenotype of Cnoc\ChR1::Csub\ChR^{CsChrimson.IVS.20xUAS.Venus}, Scer\GAL4^0273-G4

(Stern et al., 2019)

Adcy1^rut-1 is a non-suppressor of abnormal neuroanatomy | larval stage phenotype of Fak^K24/Fak^N30

(Tsai et al., 2012)

Other

Statement

Reference

Adcy1^rut-1, Vav² has abnormal neurophysiology | larval stage phenotype

(Kim et al., 2024)

Adcy1^rut-1, Epac^Δ1 has abnormal neurophysiology | larval stage phenotype

(Kim et al., 2024)

Adcy1^rut-1, Rap1^rvB1 has abnormal neurophysiology | larval stage phenotype

(Kim et al., 2024)

Adcy1^rut-1, Df(1)Exel9051/+ has abnormal neuroanatomy | third instar larval stage phenotype

(Chen and Ganetzky, 2012)

rut[+]/Adcy1^rut-1, Fak^N30/Fak^KG00304 has abnormal neuroanatomy | larval stage phenotype

(Tsai et al., 2012)

rut[+]/Adcy1^rut-1, amn^chpd has abnormal thermotaxis | dominant phenotype

(Hong et al., 2008)

Adcy1^rut-1, Pka-C1[+]/Pka-C1^B10 has abnormal thermotaxis | dominant phenotype

(Hong et al., 2008)

Phenotype Manifest In

NOT Enhanced by

Statement

Reference

Adcy1^rut-1 has phenotype, non-enhanceable by Gαs^B19

(Wolfgang et al., 2004)

NOT suppressed by

Statement

Reference

Adcy1^rut-1 has phenotype, non-suppressible by Gαs^B19

(Wolfgang et al., 2004)

NOT Enhancer of

Statement

Reference

Adcy1^rut-1 is a non-enhancer of NMJ bouton | larval stage | increased number phenotype of Fak^K24/Fak^N30

(Tsai et al., 2012)

Adcy1^rut-1 is a non-enhancer of phenotype of Gαs^B19

(Wolfgang et al., 2004)

Suppressor of

Statement

Reference

Adcy1^rut-1 is a suppressor | partially of NMJ bouton | third instar larval stage phenotype of Lapsyn^zg1

(Guan et al., 2011)

Adcy1^rut-1 is a suppressor | partially of synapse | third instar larval stage phenotype of Lapsyn^zg1

(Guan et al., 2011)

Adcy1^rut-1 is a suppressor of NMJ bouton | increased number phenotype of slo¹

(Lee and Wu, 2010)

Adcy1^rut-1 is a suppressor of neuromuscular junction phenotype of slo¹

(Lee and Wu, 2010)

Adcy1^rut-1 is a suppressor of NMJ bouton | increased number phenotype of sei²

(Lee and Wu, 2010)

Adcy1^rut-1 is a suppressor of neuromuscular junction phenotype of sei²

(Lee and Wu, 2010)

Adcy1^rut-1 is a suppressor of axon & motor neuron | conditional ts phenotype of Sh¹⁶

(Zhong and Wu, 2004)

Adcy1^rut-1 is a suppressor of phenotype of Pde4^dnc-1

(Zhong et al., 1992)

Adcy1^rut-1 is a suppressor of phenotype of Pde4^dnc-M11

(Zhong et al., 1992)

Adcy1^rut-1 is a suppressor of phenotype of Pde4^dnc-M14

(Zhong et al., 1992)

NOT Suppressor of

Statement

Reference

Adcy1^rut-1 is a non-suppressor of NMJ bouton | increased number | larval stage phenotype of Fak^K24/Fak^N30

(Tsai et al., 2012)

Adcy1^rut-1 is a non-suppressor of phenotype of Gαs^B19

(Wolfgang et al., 2004)

Other

Statement

Reference

Adcy1^rut-1, Vav² has embryonic/larval neuromuscular junction | larval stage phenotype

(Kim et al., 2024)

Adcy1^rut-1, Epac^Δ1 has embryonic/larval neuromuscular junction | larval stage phenotype

(Kim et al., 2024)

Adcy1^rut-1, Rap1^rvB1 has embryonic/larval neuromuscular junction | larval stage phenotype

(Kim et al., 2024)

Adcy1^rut-1, Df(1)Exel9051/+ has embryonic/larval neuromuscular junction | third instar larval stage phenotype

(Chen and Ganetzky, 2012)

rut[+]/Adcy1^rut-1, Fak^N30/Fak^KG00304 has NMJ bouton | increased number | larval stage phenotype

(Tsai et al., 2012)

Additional Comments

Genetic Interactions

Statement

Reference

Heterozygosity for both rut¹ and Df(1)Exel9051 results in a significant reduction in neuromuscular junction (NMJ) growth.

There is no further reduction in NMJ bouton number in double mutant rut¹, Df(1)Exel9051 homozygotes compared with Df(1)Exel9051 single mutants.

(Chen and Ganetzky, 2012)

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.

(Scheunemann et al., 2012)

rut¹/+ ; Fak^N30/Fak^KG00304 larvae show an increase in bouton number per muscle area at the neuromuscular junction compared to wild type.

(Tsai et al., 2012)

The increase in satellite bouton formation observed in Lapsyn^zg1 heterozygotes is partially suppressed in a rut¹ mutant background.

(Guan et al., 2011)

Despite their abundance in slo¹ single mutants, levels of both type B and type M satellites are suppressed in rut¹; slo¹ double mutants to wild-type levels, along with a slight reduction in mature bouton number.

rut¹; sei² double mutants display selective suppression of type M, but not type B satellites, along with drastically reduced mature bouton levels and branch formation.

(Lee and Wu, 2010)

rut¹/+; Nmdar1^EP331/Nmdar1^EP331 double mutants exhibit significantly lower performance in standard Pavlovian learning assays compared to either single mutant.

(Qin and Dubnau, 2010)

Scer\GAL4^c747-mediated expression of Rdl^{dsRNA.2-7.Scer\UAS} or Rdl^{dsRNA.4-5.Scer\UAS} does not suppress the low learning performance of rut¹ flies after aversive olfactory conditioning or after appetitive olfactory conditioning.

(Liu et al., 2009)

Double heterozygotes for amn^chpd and rut¹ show an inability to find a preferred temperature, with temperature preference spread across a wide gradient.

Double heterozygotes for rut¹ and Pka-C1^B10 show an inability to find a preferred temperature, with temperature preference spread across a wide gradient.

(Hong et al., 2008)

rut¹; Nf1^P2 mutants do not exhibit shorter life spans compared to rut¹ single mutants.

Mitochondrial aconitase activities in 30-day old rut¹; Nf1^P2 flies are reduced by 76% compared to controls (and 36% in Nf1^P2).

Superoxide levels are increased in rut¹; Nf1^P2 flies compared to controls.

(Tong et al., 2007)

The addition of rut¹ to G-sα60A^B19 larvae has no effect on synapse formation.

(Wolfgang et al., 2004)

The increased arborization of motor axon terminals seen when both Sh¹²⁰ and Sh¹⁶ larvae are raised at 25^oC is partially suppressed in rut¹, Sh¹²⁰ and rut¹, Sh¹⁶ double mutant larvae.

(Zhong and Wu, 2004)

The learning scores of rut¹; Nf1^P2 double mutant flies are similar to that of either single mutant.

(Guo et al., 2000)

Xenogenetic Interactions

Statement

Reference

Flies overexpressing Hsap\APP^{Aβ1-42.Scer\UAS.cIa} driven by Scer\GAL4^Cha.7.4 in a rut¹ mutant background display age-dependent progressive locomotor dysfunction significantly earlier than Hsap\APP^{Aβ1-42.Scer\UAS.cIa}-overexpressing flies without rut¹ in the genetic background.

(Iijima-Ando et al., 2009)

Complementation and Rescue Data

Fails to complement

Adcy1^rut-178

(Martin et al., 2001)

Adcy1^MB2769

(Han et al., 1992)

Adcy1^rut-2080

(Levin et al., 1992)

Adcy1^rut-178

(Levin et al., 1992)

Adcy1^rut-1084

(Levin et al., 1992)

Rescued by

Adcy1^rut-1 is rescued by Scer\GAL4^ey-OK107/Adcy1^UAS.cZa

(Scheunemann et al., 2012)

Adcy1^rut-1 is rescued by Scer\GAL4^Mef2.247/Adcy1^UAS.cZa

(Scheunemann et al., 2012)

Partially rescued by

Adcy1^rut-1 is partially rescued by Adcy1^UAS.cHa/Scer\GAL4^Mef2.247

(Hong et al., 2008)

Adcy1^rut-1 is partially rescued by Adcy1^UAS.cHa/Scer\GAL4^c309

(Hong et al., 2008)

Not rescued by

Adcy1^rut-1 is not rescued by Adcy1^UAS.cZa/Scer\GAL4^17d

(Scheunemann et al., 2012)

Adcy1^rut-1 is not rescued by Adcy1^UAS.cZa/Scer\GAL4^NP1131

(Scheunemann et al., 2012)

Adcy1^rut-1 is not rescued by Adcy1^UAS.cZa/Scer\GAL4^c320

(Scheunemann et al., 2012)

Adcy1^rut-1 is not rescued by Scer\GAL4^c305a/Adcy1^UAS.cZa

(Scheunemann et al., 2012)

Comments

Expression of rut^Scer\UAS.cZa under the control of Scer\GAL4^ey-OK107 or Scer\GAL4^Mef2.247, but not Scer\GAL4^17d, Scer\GAL4^NP1131, Scer\GAL4^c320, or Scer\GAL4^c305a, rescues the defective short term memory performance of rut¹/rut¹ mutants.

Expression of rut^Scer\UAS.cZa under the control of Scer\GAL4^Mef2.247, but not Scer\GAL4^17d or Scer\GAL4^NP1131, rescues the defective anaethesia-sensitive memory performance of rut¹/rut¹ mutants.

(Scheunemann et al., 2012)

Expression of rut^Scer\UAS.cHa under the control of either Scer\GAL4^Mef2.247 or Scer\GAL4^c309 almost completely rescues the temperature preference behavior defects seen in rut¹ mutant.

(Hong et al., 2008)

Images (0)

Mutant

Wild-type

Stocks (4)

Bloomington

9404

Adcy1^rut-1

6350

sc^e Adcy1^rut-1 f⁵ Sh¹⁴/C(1)DX, y¹ w¹ f¹

Kyoto

108747