FlyBase Allele Report: Dmel\eag[1]

General Information

Symbol

Dmel\eag¹

Species

D. melanogaster

Name

FlyBase ID

FBal0003484

Feature type

allele

Associated gene

Dmel\eag

Associated Insertion(s)

Carried in Construct

Also Known As

eag

Key Links

Allele class

hypomorphic allele - genetic evidence

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

hypomorphic allele - genetic evidence

(Wang et al., 2002)

Mutagen

ethyl methanesulfonate

(Broadie and Bate, 1993, Budnik et al., 1990)

Progenitor genotype

Cytology

Description

Encodes a protein with a truncated C-terminus.

(Wang et al., 2002)

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 epilepsy

CEA

(Fergestad et al., 2006)

CEA with Sh¹⁴

(Fergestad et al., 2006)

CEA with Sh¹²⁰

(Li et al., 2021)

Modifiers Based on Experimental Evidence ( 1 )

Disease

Interaction

References

ameliorates brain cancer

modeled by dpn^UAS.cWa

(Huang et al., 2015)

model of epilepsy

is exacerbated by Atpα^DTS1

(Fergestad et al., 2006)

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

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

adult brain

(Fergestad et al., 2006)

leg

(Hurd et al., 1996)

neuromuscular junction

(Schuster et al., 1996, Broadie and Bate, 1993)

synapse

(Schuster et al., 1996, Griffith et al., 1994, Broadie and Bate, 1993)

Detailed Description

Statement

Reference

Homozygous eag¹ significantly blocks or reduces tolerance to both benzyl alcohol and ethanol.

(Ghezzi et al., 2013)

eag¹ flies do not show a significantly shortened lifespan. At day 33, the brains of these flies show intermittent pathology.

(Fergestad et al., 2006)

At room temperature, the motor axon terminals of eag¹ larvae show a similar level of arborization to wild-type larvae.

(Zhong and Wu, 2004)

eag¹ flies show normal osmotic stress sensitivity on food medium containing NaCl.

(Huang et al., 2002)

The seizure threshold following short wavetrains of high-frequency electrical stimuli (0.5ms pulses at 200Hz for 300ms) is increased in mutant flies (62.1 +/- 10.3 V) compared to controls.

The threshold for activation of the giant fiber in mutant animals following single stimulus pulses (0.2ms duration, 0.5Hz) is not significantly different from that of wild type.

(Kuebler et al., 2001)

The resting potentials of mutant dorsolongitudinal muscles does not differ significantly from wild type at 22 or 12^oC.

(Hosler et al., 2000)

When exposed to 10mM paraquat for 48hr, mutants show 48% survival (wild type shows 97% survival).

(Wang et al., 2000)

Mutant larvae show a reduction in heart rate.

(Robbins et al., 1999)

Homozygous adults show a reduced response to propionic acid, ethyl butyrate, 2-butanone and ethyl acetate in an electroantennogram assay compared to control flies. The response to butanol, 1-octanol, benzaldehyde, butyl acetate and 2-heptanone in this assay is not significantly different from the response of control flies to these odorants. Mutant flies have fewer antennal neurons that are sensitive to ethyl butyrate than control flies. The proportion of antennal olfactory neurons that are responsive to membrane-permeant cyclic nucleotide analogues (8-Br-cAMP and 8-Br-cGMP) is also reduced in mutant flies compared to wild-type.

(Dubin et al., 1998)

The rate of habituation of the giant fiber escape pathway is increased and the number of stimuli needed to attain five consecutive failures is decreased in eag¹ flies compared to wild-type. The short-latency response of the dorsal longitudinal muscle occurs earlier than in wild-type flies. The rate of habituation in Sh²¹ eag¹ double mutants is no more extreme than in Sh²¹ or eag¹ single mutants.

(Engel and Wu, 1998)

Homozygous adults are more sensitive to paraquat than control flies. Homozygous adults have a reduced lifespan compared to wild-type flies.

(Humphreys et al., 1996)

eag¹/Sh⁷ double mutants cause an increase in neuronal excitability and result in a postembryonic increase in structure (both number of boutons and branches) at the larval neuromuscular junction (NMJ). Bursting pattern of motor neuron action potentials controlling larval locomotion shows near constant activity. Excitatory postsynaptic potentials (EPSP) reveal defective nerve repolarisation. Number of boutons in eag¹/Sh⁷ double mutants is increased compared to wild type due to reduction in Fas2 expression. Bouton number does not increase when Fas2^Scer\UAS.cLa is expressed from Scer\GAL4^E62-2 in eag¹/Sh⁷ larvae.

(Schuster et al., 1996)

Homozygotes show increased sensitivity to chloroform and trichloroethylene in an inebriometer assay (an assay of geotactic and postural behaviour) compared to wild-type flies. Sensitivity of homozygotes to halothane is not significantly different to wild-type flies, but heterozygotes show slight resistance to halothane compared to wild-type.

(Leibovitch et al., 1995)

Hemizygotes fail to show courtship conditioning, showing an increase in courtship of mated females compared to wild type controls. Physiological studies reveal supernumerary synaptic discharges.

(Griffith et al., 1994)

Individuals exhibit clear free-running locomotor activity rhythms.

(Levine et al., 1994)

Mutation dramatically increases the number of excitatory junction potentials (EJP) at the larval neuromuscular junction (NMJ) (FBrf0039808). eag¹ Sh¹⁴ double mutant embryos show greatly increased synaptic activity, both the burst frequency and the mean excitatory junction current (EJC) amplitude are increased during synaptogenesis. The synaptic morphology of the double mutant embryonic NMJs raised at the restrictive temperature are not significantly different from wild type, at the light microscope level. These hyperactive synapses expand to occupy a larger area of the muscle surface relative to wild type causing decreased synaptic density (the branch and bouton numbers are not altered).

(Broadie and Bate, 1993)

eag¹ Sh²¹ double hemizygous bristle sensory cells in small-patch mosaic adult flies are more responsive to tactile stimulation than wild-type bristles, although the pathfinding and formation of sensory cell projections is normal.

(Burg et al., 1993)

eag¹, Sh¹⁴ double mutants have normal grooming behavior.

(Phillis et al., 1993)

Response of the channel to modulation by protein kinases depends on temperature: I_A is increased at 5^oC but remains almost unchanged at 16^oC, conversely I_K is nearly normal at 5^oC and decreased at 16^oC. At 16^oC I_A and I_K levels, and I_CF and I_CS levels can be reduced by application of W7, a Ca²⁺/CaM antagonist. cGMP-modulation of I_K and I_A by the mutant channel by 8-Br-cGMP is altered.

(Zhong and Wu, 1993)

Flies show some leg-shaking under anaesthesia. The action potential of the dorsal longitudinal muscle often appears abnormal in Sh¹⁴ eag¹ double mutants. The action potential of the dorsal longitudinal muscle occasionally appears abnormal in eag¹ mutants. Lowers the following frequency of the giant fibre response of the tergotrochanteral muscle pathway. eag¹ Sh²¹ and eag¹ Sh¹⁴ double mutant flies show spontaneous activity of the dorsal longitudinal and dorsoventral indirect flight muscles when at rest. This phenotype is suppressed by mle^nap-ts1 in eag¹ Sh²¹ mle^nap-ts1 flies. 86% of eag¹ Sh¹⁴ flies have a wings-down phenotype.

(Engel and Wu, 1992)

No effect on synaptic currents at neuromuscular junction of third instar larvae.

(Gho and Ganetzky, 1992)

The mutants effects 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.

(Zhong et al., 1992)

Defects in all K⁺ currents within larval muscle.

(Zhong and Wu, 1991)

Recessive mutation. eag¹ Sh¹⁴ double mutant larvae show an increased number of tertiary and quarternary axonal branches over muscles 12 and 13. The number, and in some cases density, of varicosities in the neurites is also increased. eag¹ Hk¹ double mutant larvae have a similar phenotype. eag¹ Hk¹ double mutant larval muscles show periods of activity not organised into bursts (tonic activity) in contrast to wild-type.

(Budnik et al., 1990)

eag¹ males show conditioned courtship behaviour like wild-type males, but the refractory period is abnormally short.

(Cowan and Siegel, 1984)

Homozygous flies have a high frequency of spontaneous excitatory junction potentials (ejps). eag¹ interacts synergistically with either Sh¹⁴ or Sh²¹ in double mutants to produce extremely prolonged neuromuscular transmission and spontaneous firing of the motor axons. eag¹ larvae treated with 4-aminopyridine show a striking enhancement of the amplitude and duration of the ejp, and they also show spontaneous ejps.

(Ganetzky and Wu, 1983)

Abnormal leg shaking under ether anaesthesia; aberrant, repetitive firing of action potentials in larval nerves; potassium currents abnormal in larval muscles (Wu, Ganetzky, Haugland and Lin, 1983). eag Sh double mutants display greatly increased level of spontaneous neuronal activity and extreme behavioral phenotypes (Burg and Wu, 1989).

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

eag¹ has chemical sensitive phenotype, enhanceable by Hk¹

(Wang et al., 2000)

eag¹ has chemical sensitive phenotype, enhanceable by qvr¹

(Wang et al., 2000)

eag¹ has visible phenotype, enhanceable by qvr¹

(Wang et al., 2000)

eag¹ has chemical sensitive phenotype, enhanceable by Sh²¹

(Wang et al., 2000)

NOT Enhanced by

Statement

Reference

Sh¹⁴, eag¹ has short lived phenotype, non-enhanceable by Atpα^DTS1/Atpα^DTS1

(Fergestad et al., 2006)

Suppressed by

Statement

Reference

Sh²¹, eag¹ has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by LanA^C01-190/Scer\GAL4^C57

(Tsai et al., 2012)

Sh²¹, eag¹ has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by Scer\GAL4^Toll-6-D42/Itgbn^UAS.cTa

(Tsai et al., 2012)

Sh²¹, eag¹ has chemical sensitive phenotype, suppressible | partially by mle^nap-ts1

(Wang et al., 2000)

eag¹ has abnormal behavior | recessive phenotype, suppressible by Khc^1ts

(Hurd et al., 1996)

eag¹ has abnormal behavior | recessive phenotype, suppressible by Khc⁶/Khc^BD

(Hurd et al., 1996)

Enhancer of

Statement

Reference

eag¹ is an enhancer of chemical sensitive phenotype of Hk¹

(Wang et al., 2000)

eag¹ is an enhancer of chemical sensitive phenotype of qvr¹

(Wang et al., 2000)

eag¹ is an enhancer of visible phenotype of qvr¹

(Wang et al., 2000)

eag¹ is an enhancer of chemical sensitive phenotype of Sh²¹

(Wang et al., 2000)

NOT Enhancer of

Statement

Reference

eag[+]/eag¹ is a non-enhancer of short lived | dominant phenotype of Atpα^DTS1

(Fergestad et al., 2006)

Suppressor of

Statement

Reference

eag¹ is a suppressor of abnormal neuroanatomy | third instar larval stage phenotype of Scer\GAL4^insc-Mz1407, dpn^UAS.cWa

(Huang et al., 2015)

eag¹ is a suppressor | partially of lethal - all die before end of larval stage | heat sensitive phenotype of Scer\GAL4^insc-Mz1407, dpn^UAS.cWa

(Huang et al., 2015)

Other

Statement

Reference

Sh²¹, eag¹ has abnormal neuroanatomy | third instar larval stage phenotype

(Tsai et al., 2012)

Sh¹⁴, eag¹ has short lived phenotype

(Fergestad et al., 2006)

Sh²¹, eag¹ has abnormal neuroanatomy phenotype

(Hebbar and Fernandes, 2005)

Sh²¹, eag¹ has increased rate of movement phenotype

(Hebbar and Fernandes, 2005)

Sod1ⁿ¹, eag¹ has viable phenotype

(Humphreys et al., 1996)

Sh²¹, eag¹ has abnormal behavior phenotype

(Zhong and Wu, 1993)

Sh⁵, eag¹ has visible phenotype

(Zhong and Wu, 1993)

Sh⁵, eag¹ has abnormal behavior phenotype

(Zhong and Wu, 1993)

Sh²¹, eag¹ has visible phenotype

(Zhong and Wu, 1993)

Phenotype Manifest In

Enhanced by

Statement

Reference

eag¹ has wing phenotype, enhanceable by qvr¹

(Wang et al., 2000)

Suppressed by

Statement

Reference

Sh²¹, eag¹ has neuromuscular junction | third instar larval stage phenotype, suppressible by LanA^C01-190/Scer\GAL4^C57

(Tsai et al., 2012)

Sh²¹, eag¹ has neuromuscular junction | third instar larval stage phenotype, suppressible by Scer\GAL4^Toll-6-D42/Itgbn^UAS.cTa

(Tsai et al., 2012)

Sh²¹, eag¹ has synapse | ectopic phenotype, suppressible by Gαs^B19

(Wolfgang et al., 2004)

eag¹ has phenotype, suppressible by Khc⁴

(Hurd et al., 1996)

eag¹ has phenotype, suppressible by Khc⁵

(Hurd et al., 1996)

eag¹ has leg phenotype, suppressible by Khc^1ts

(Hurd et al., 1996)

eag¹ has leg phenotype, suppressible by Khc⁶/Khc^BD

(Hurd et al., 1996)

Enhancer of

Statement

Reference

eag¹ is an enhancer of CNS surface glial cell phenotype of Nf1^P2

(Yager et al., 2001)

eag¹ is an enhancer of wing phenotype of qvr¹

(Wang et al., 2000)

Suppressor of

Statement

Reference

eag¹ is a suppressor of type I neuroblast | third instar larval stage phenotype of Scer\GAL4^insc-Mz1407, dpn^UAS.cWa

(Huang et al., 2015)

eag¹ is a suppressor of type II neuroblast | third instar larval stage phenotype of Scer\GAL4^insc-Mz1407, dpn^UAS.cWa

(Huang et al., 2015)

Other

Statement

Reference

Sh²¹, eag¹ has neuromuscular junction | third instar larval stage phenotype

(Tsai et al., 2012)

Scer\GAL4^Tdc2.PC, Sh^SDN.UAS, eag¹ has embryonic/larval neuromuscular junction phenotype

(Koon et al., 2011)

Scer\GAL4^Tdc2.PC, Sh^SDN.UAS, eag¹ has multidendritic neuron | third instar larval stage phenotype

(Koon et al., 2011)

Scer\GAL4^Tdc2.PC, Sh^SDN.UAS, eag¹ has type II bouton | third instar larval stage phenotype

(Koon et al., 2011)

Sh²¹, eag¹ has indirect flight muscle motor neuron DLMN5 phenotype

(Hebbar and Fernandes, 2005)

Sh²¹, eag¹ has neuromuscular junction phenotype

(Hebbar and Fernandes, 2005)

Scer\GAL4^{elav.Switch.PO}, Sh^{DN.EKI.UAS.GFP(GL)}, eag¹ has NMJ bouton | increased number phenotype

(Mosca et al., 2005)

Sh²¹, eag¹ has synapse | ectopic phenotype

(Wolfgang et al., 2004)

Sh¹²⁰, eag¹ has axon & motor neuron phenotype

(Zhong and Wu, 2004)

eag¹, poe² has CNS surface glial cell phenotype

(Yager et al., 2001)

eag¹, poe¹ has CNS surface glial cell phenotype

(Yager et al., 2001)

Appl^sd.UAS, Scer\GAL4^unspecified, Sh¹⁴, eag¹ has bouton phenotype

(Torroja et al., 1999)

Sh⁵, eag¹ has wing phenotype

(Zhong and Wu, 1993)

Sh²¹, eag¹ has wing phenotype

(Zhong and Wu, 1993)

Sh²¹, eag¹ has anterior postalar bristle phenotype

(Burg and Wu, 1989)

Sh²¹, eag¹ has posterior supraalar bristle phenotype

(Burg and Wu, 1989)

Additional Comments

Genetic Interactions

Statement

Reference

eag¹ mutant third instar larvae display markedly reduces dpn^Scer\UAS.cWa-induced tumor growth.

(Huang et al., 2015)

eag¹ Sh²¹ double mutant third instar larvae show overgrowth of the neuromuscular junction. This overgrowth is significantly suppressed by expression of either LanA^C01-190 under the control of Scer\GAL4^C57 or βInt-ν^Scer\UAS.cTa under the control of Scer\GAL4^D42.

(Tsai et al., 2012)

Expression of Sh^SDN.Scer\UAS under the control of Scer\GAL4^Tdc2.PC in type II neurons in an eag¹ mutant background results in an increase in the number of natural synaptopods and type II boutons and terminal branches.

(Koon et al., 2011)

eag¹ Sh¹⁴ flies show ether-sensitive leg-shaking behavior, which is not suppressed by expression of dao^Scer\UAS.cFa under the control of Scer\GAL4^unspecified.

(Fergestad et al., 2010)

eag¹, Sh¹⁴ flies become severely uncoordinated with age and show a significantly shortened lifespan (<1 week). No gross pathology is ever observed in the brains of these double mutants. There is no additional reduction in lifespan in eag¹, Sh¹⁴; Atpα^DTS1 triple mutants compared to eag¹, Sh¹⁴ mutants. eag¹/+; Atpα^DTS1/+ double mutants have a similar lifespan to Atpα^DTS1/+ single mutants.

(Fergestad et al., 2006)

There is an increase in the number and density of secondary branches along the primary branches of the motor neuron that innervates DLMa in eag¹/Sh²¹ mutants. The length of these secondary branches is not affected, but 75% of mutants have less than the wild-type number of contact points between the neuron and the muscle.

(Hebbar and Fernandes, 2005)

When Sh^{SDN.Scer\UAS.T:Avic\GFP-GL} is driven by Scer\GAL4^{Mhc.Switch.PO} in a eag¹ and mutants are exposed to RU486 no effect is seen on arborisation. If driven by Scer\GAL4^{elav.Switch.PO} in a eag¹ background synaptic arbor growth is significantly increased. The mean bouton count in NMJ boutons is almost doubled in these mutants.

(Mosca et al., 2005)

eag¹, Sh¹²⁰; mGluRA^112b show the neuromuscular junction overgrowth phenotype of eag¹, Sh¹²⁰ double mutants.

(Bogdanik et al., 2004)

eag¹. Sh²¹ mutants exhibit a synaptic over-growth phenotype. The addition of G-sα60A^B19 suppresses this phenotype.

(Wolfgang et al., 2004)

eag¹, Sh¹⁶ double mutant larvae show an enhanced level of motor axon terminal arborization compared to wild-type larvae, when raised at room temperature. No such increase is seen in either single mutant at this temperature.

(Zhong and Wu, 2004)

The addition of poe¹ or poe² to eag¹ mutants leads to strongly potentiated perineural glial growth. The addition of ine¹ to eag¹ has no effect on the perineurial glial cells.

(Yager et al., 2001)

100% of eag¹, qvr¹ double mutants hold their wings down, similar to those of eag,Sh double mutants.

(Wang et al., 2000)

When Appl^sd.Scer\UAS expression is driven in the motoneurons muscles 6 and 7 (abdominal segment 3) in combination with eag¹, Sh¹⁴ total number of synaptic boutons is decreased compared to Appl^sd.Scer\UAS alone, percentage of satellite boutons is decreased compared to Appl^sd.Scer\UAS alone and the number of normal boutons is increased compared to Appl^sd.Scer\UAS alone.

(Torroja et al., 1999)

Khc⁶/Khc^BD suppresses the leg shaking of eag¹ mutants, and this phenotype is reversed by addition of one copy of Khc^+t7.5.

(Hurd et al., 1996)

eag¹/Rat\CamKII-I^Ala.hs individuals also fail to court.

(Griffith et al., 1994)

eag¹ Sh⁵ and eag¹ Sh²¹ double mutants exhibit vigorous leg-shaking behaviour under ether anaesthesia. Many exhibit a wings down phenotype. High frequency, spontaneous EJPs of a greater amplitude are seen at larval neuromuscular junctions and spontaneous discharges of EJPs or action potentials can be recorded in adult flight muscles.

(Zhong and Wu, 1993)

eag¹, Sh²¹ double hemizygous males show ether-induced violent leg shaking. Analysis of eag¹, Sh²¹ mosaics shows that bristles not normally responsive to mechanical stimulation, such as the anterior postalar and posterior supraalar sensory cells, become much more sensitive to mechanical stimulation in the double mutant.

(Burg and Wu, 1989)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Comments

Images (0)

Mutant

Wild-type

Stocks (2)

3561

107098

Notes on Origin

Discoverer

Comments

eag¹ Sh¹⁴ double mutants significantly reduce postsynaptic expression of GluRIIA by the end of embryogenesis.

(Broadie and Bate, 1993)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (2)

Reported As

Symbol Synonym

Name Synonyms

Secondary FlyBase IDs

References (62)

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