Allele Dmel\rut¹

General Information
Symbol	Dmel\rut¹	Species	D. melanogaster
Name		FlyBase ID	FBal0014878
Feature type	allele	Associated gene	Dmel\rut

Allele class	loss of function allele
Mutagen	ethyl methanesulfonate
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class	loss of function allele (Zhong and Wu, 2004)
Mutagen	ethyl methanesulfonate (Feany, 1990)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference Single point mutation substituting adenine for guanine at position 3459, corresponding to arginine substituted for glycine at amino acid 1026. (Levin et al., 1992)
Cytology
Phenotypic Data
Phenotypic Class
	behavior defective \| recessive (Phillis et al., 1993) chemical sensitive (Moore et al., 1998) learning defective (Guo et al., 2000, Honjo and Furukubo-Tokunaga, 2009) memory defective (Honjo and Furukubo-Tokunaga, 2005, Blum et al., 2009, Honjo and Furukubo-Tokunaga, 2009, Tan et al., 2010, Qin and Dubnau, 2010) memory defective (with rut²⁰⁸⁰) (Blum et al., 2009) neuroanatomy defective (Shayan and Atwood, 2000, Renger et al., 2000) neuroanatomy defective \| larval stage (Bhattacharya et al., 1999) neuroanatomy defective \| third instar larval stage (Guan et al., 2011, Chen and Ganetzky, 2012) neurophysiology defective (Martin et al., 2001, Hou et al., 2003, Renger et al., 2000, Kuromi and Kidokoro, 2000) neurophysiology defective \| larval stage (Bhattacharya et al., 1999) smell perception defective (Martin et al., 2001, Honjo and Furukubo-Tokunaga, 2005, Xia and Tully, 2007) taste perception defective (Honjo and Furukubo-Tokunaga, 2005)
Phenotype Manifest In
	axon & motor neuron \| conditional ts (Zhong and Wu, 2004) axon \| third instar larval stage (Guan et al., 2011) dense body (Shayan and Atwood, 2000) embryonic/larval neuromuscular junction \| third instar larval stage (Chen and Ganetzky, 2012) mushroom body calyx (Hitier et al., 1998) neuromuscular junction (Shayan and Atwood, 2000, Renger et al., 2000, Kuromi and Kidokoro, 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 (Shayan and Atwood, 2000, Renger et al., 2000) varicosity \| third instar larval stage (Guan et al., 2011)
Detailed Description
	Statement Reference rut[1] causes a mild neuromuscular junction (NMJ) undergrowth phenotype. Heterozygous rut[1] larvae have NMJs that do not differ from wild-type. (Chen and Ganetzky, 2012) Compared with wild-type, rut[1] 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) rut[1] mutants do not display any changes in synaptic morphology compared to wild-type. (Lee and Wu, 2010) rut[1] 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 rut[1]/rut[2080] 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 rut[1] mutant larvae. (Honjo and Furukubo-Tokunaga, 2009) rut[1] mutants exhibit significantly shorter life spans compared to controls. rut[1] 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 rut[1] flies are reduced by 75% compared to controls. Superoxide levels are increased in rut[1] flies compared to controls. (Tong et al., 2007) Homozygous rut[1] mutants exhibit normal spontaneous odor identity discrimination. Homozygous rut[1] 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) 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 the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement Reference rut¹ has memory defective phenotype, enhanceable by Nmdar1^EP331 (Qin and Dubnau, 2010)
Enhancer of
Statement Reference rut[+]/rut¹ is an enhancer of memory defective phenotype of Nmdar1^EP331 (Qin and Dubnau, 2010) rut¹ is an enhancer of locomotor behavior defective phenotype of Hsap\APP^{Aβ1-42.Scer\UAS.cIa}, Scer\GAL4^Cha.7.4 (Iijima-Ando et al., 2009)
Suppressor of
Statement Reference rut¹ is a suppressor \| partially of neuroanatomy defective \| dominant \| third instar larval stage phenotype of Lapsyn^zg1 (Guan et al., 2011) rut¹ is a suppressor of neuroanatomy defective phenotype of sei² (Lee and Wu, 2010) rut¹ is a suppressor of neuroanatomy defective phenotype of slo¹ (Lee and Wu, 2010)
Other
Statement Reference Df(1)Exel9051, Df(1)Exel9051, +, rut¹ has neuroanatomy defective \| third instar larval stage phenotype (Chen and Ganetzky, 2012)
Phenotype Manifest In
NOT Enhanced by
Statement Reference rut¹ has phenotype, non-enhanceable by Gαs^B19 (Wolfgang et al., 2004)
NOT suppressed by
Statement Reference rut¹ has phenotype, non-suppressible by Gαs^B19 (Wolfgang et al., 2004)
NOT Enhancer of
Statement Reference rut¹ is a non-enhancer of phenotype of Gαs^B19 (Wolfgang et al., 2004)
Suppressor of
Statement Reference rut¹ is a suppressor \| partially of axon & motor neuron \| conditional ts phenotype of Sh¹⁶ (Zhong and Wu, 2004) rut¹ is a suppressor \| partially of NMJ bouton \| third instar larval stage phenotype of Lapsyn^zg1 (Guan et al., 2011) rut¹ is a suppressor \| partially of synapse \| third instar larval stage phenotype of Lapsyn^zg1 (Guan et al., 2011) rut¹ is a suppressor of neuromuscular junction phenotype of sei² (Lee and Wu, 2010) rut¹ is a suppressor of neuromuscular junction phenotype of slo¹ (Lee and Wu, 2010) rut¹ is a suppressor of NMJ bouton \| supernumerary phenotype of sei² (Lee and Wu, 2010) rut¹ is a suppressor of NMJ bouton \| supernumerary phenotype of slo¹ (Lee and Wu, 2010) rut¹ is a suppressor of phenotype of dnc¹ (Zhong et al., 1992) rut¹ is a suppressor of phenotype of dnc^M11 (Zhong et al., 1992) rut¹ is a suppressor of phenotype of dnc^M14 (Zhong et al., 1992)
NOT Suppressor of
Statement Reference rut¹ is a non-suppressor of phenotype of Gαs^B19 (Wolfgang et al., 2004)
Other
Statement Reference Df(1)Exel9051, Df(1)Exel9051, +, rut¹ has embryonic/larval neuromuscular junction \| third instar larval stage phenotype (Chen and Ganetzky, 2012)
Additional Comments
Genetic Interactions
Statement Reference Heterozygosity for both rut[1] 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 rut[1], Df(1)Exel9051 homozygotes compared with Df(1)Exel9051 single mutants. (Chen and Ganetzky, 2012) The increase in satellite bouton formation observed in Lapsyn[zg1] heterozygotes is partially suppressed in a rut[1] mutant background. (Guan et al., 2011) Despite their abundance in slo[1] single mutants, levels of both type B and type M satellites are suppressed in rut[1]; slo[1] double mutants to wild-type levels, along with a slight reduction in mature bouton number. rut[1]; sei[2] 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) rut[1]/+; Nmdar1[EP331]/Nmdar1[EP331] double mutants exhibit significantly lower performance in standard Pavlovian learning assays compared to either single mutant. (Qin and Dubnau, 2010) rut[1]; Nf1[P2] mutants do not exhibit shorter life spans compared to rut[1] single mutants. Mitochondrial aconitase activities in 30-day old rut[1]; Nf1[P2] flies are reduced by 76% compared to controls (and 36% in Nf1[P2]). Superoxide levels are increased in rut[1]; 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 rut[1] mutant background display age-dependent progressive locomotor dysfunction significantly earlier than Hsap\APP[Aβ1-42.Scer\UAS.cIa]-overexpressing flies without rut[1] in the genetic background. (Iijima-Ando et al., 2009)
Complementation & Rescue Data
Fails to complement	rut¹⁷⁸ (Martin et al., 2001, Levin et al., 1992) rut¹⁰⁸⁴ (Levin et al., 1992) rut²⁰⁸⁰ (Levin et al., 1992) rut^MB2769 (Han et al., 1992)
Comments
Stocks ( 4 )
Bloomington	9404 rut¹ 6350 sc^e rut¹ f⁵ Sh¹⁴/C(1)DX, y¹ w¹ f¹
Kyoto	108747 sc^e rut¹ f⁵ Sh¹⁴/C(1)DX, y¹ f¹ 102048 sc^e rut¹ f⁵ Sh¹⁴ / C(1)DX, y¹ f¹
Notes on Origin
Discoverer	Sziber.

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 2 )
Reported As
Symbol Synonym	rut¹ (Guo and Zhong, 2006, Zhong and Wu, 2004, Mee et al., 2004, Honjo and Furukubo-Tokunaga, 2005, Aravamudan and Broadie, 2003, Guan et al., 2011, Blum et al., 2009, Honjo and Furukubo-Tokunaga, 2009, Xia and Tully, 2007, Iijima-Ando et al., 2009, Tan et al., 2010, Lee and Wu, 2010, Kang et al., 2011, Tong et al., 2007, Chen and Ganetzky, 2012)
Name Synonym	rutabaga1 (Qin and Dubnau, 2010)
Secondary FlyBase IDs

References ( 51 )

Generate a list of	All references relating to this allele ( 51 )

List References by type	Research paper ( 47 ) Review ( 3 ) Abstract ( 1 )
Recent research papers ( 3 )
	Chen and Ganetzky, 2012, J. Cell Biol. 196(4): 529--543 A neuropeptide signaling pathway regulates synaptic growth in Drosophila. [FBrf0217500] Guan et al., 2011, Learn. Mem. 18(4): 191--206 Altered gene regulation and synaptic morphology in Drosophila learning and memory mutants. [FBrf0213277] Kang et al., 2011, PLoS ONE 6(12): e29800 Novel Cytochrome P450, cyp6a17, Is Required for Temperature Preference Behavior in Drosophila. [FBrf0217065] Show all research papers ...
Recent reviews (0)
	All reviews listed in FlyBase were published before 2011 Show reviews ...

Allele Dmel\rut1

Allele Dmel\rut¹