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General Information
Symbol
Dmel\eag1
Species
D. melanogaster
Name
FlyBase ID
FBal0003484
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
eag
Key Links
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

Encodes a protein with a truncated C-terminus.

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
Modifiers Based on Experimental Evidence ( 1 )
Disease
Interaction
References
ameliorates  brain cancer
model of  epilepsy
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

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

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

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

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

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.

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

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

Mutant larvae show a reduction in heart rate.

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.

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.

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

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 Fas2Scer\UAS.cLa is expressed from Scer\GAL4E62-2 in eag1/Sh7 larvae.

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.

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.

Individuals exhibit clear free-running locomotor activity rhythms.

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).

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.

eag1, Sh14 double mutants have normal grooming behavior.

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

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 mlenap-ts1 in eag1 Sh21 mlenap-ts1 flies. 86% of eag1 Sh14 flies have a wings-down phenotype.

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

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.

Defects in all K+ currents within larval muscle.

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.

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

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.

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
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference

eag1 has chemical sensitive phenotype, enhanceable by Hk1

eag1 has chemical sensitive phenotype, enhanceable by qvr1

eag1 has visible phenotype, enhanceable by qvr1

eag1 has chemical sensitive phenotype, enhanceable by Sh21

NOT Enhanced by
Statement
Reference

Sh14, eag1 has short lived phenotype, non-enhanceable by AtpαDTS1/AtpαDTS1

Suppressed by
Enhancer of
Statement
Reference

eag1 is an enhancer of chemical sensitive phenotype of Hk1

eag1 is an enhancer of chemical sensitive phenotype of qvr1

eag1 is an enhancer of visible phenotype of qvr1

eag1 is an enhancer of chemical sensitive phenotype of Sh21

NOT Enhancer of
Statement
Reference

eag[+]/eag1 is a non-enhancer of short lived | dominant phenotype of AtpαDTS1

Suppressor of
Other
Phenotype Manifest In
Enhanced by
Statement
Reference

eag1 has wing phenotype, enhanceable by qvr1

Suppressed by
Statement
Reference

Sh21, eag1 has synapse | ectopic phenotype, suppressible by GαsB19

eag1 has leg phenotype, suppressible by Khc1ts

eag1 has phenotype, suppressible by Khc4

eag1 has phenotype, suppressible by Khc5

eag1 has leg phenotype, suppressible by Khc6/KhcBD

Enhancer of
Statement
Reference

eag1 is an enhancer of wing phenotype of qvr1

Suppressor of
Other
Additional Comments
Genetic Interactions
Statement
Reference

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

eag1 Sh21 double mutant third instar larvae show overgrowth of the neuromuscular junction. This overgrowth is significantly suppressed by expression of either LanAC01-190 under the control of Scer\GAL4C57 or βInt-νScer\UAS.cTa under the control of Scer\GAL4D42.

Expression of ShSDN.Scer\UAS under the control of Scer\GAL4Tdc2.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.

eag1 Sh14 flies show ether-sensitive leg-shaking behavior, which is not suppressed by expression of daoScer\UAS.cFa under the control of Scer\GAL4unspecified.

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; AtpαDTS1 triple mutants compared to eag1, Sh14 mutants. eag1/+; AtpαDTS1/+ double mutants have a similar lifespan to AtpαDTS1/+ single mutants.

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.

When ShSDN.Scer\UAS.T:Avic\GFP-GL is driven by Scer\GAL4Mhc.Switch.PO in a eag1 and mutants are exposed to RU486 no effect is seen on arborisation. If driven by Scer\GAL4elav.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.

eag1, Sh120; mGluRA112b show the neuromuscular junction overgrowth phenotype of eag1, Sh120 double mutants.

eag1. Sh21 mutants exhibit a synaptic over-growth phenotype. The addition of G-sα60AB19 suppresses this phenotype.

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.

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.

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

When Applsd.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 Applsd.Scer\UAS alone, percentage of satellite boutons is decreased compared to Applsd.Scer\UAS alone and the number of normal boutons is increased compared to Applsd.Scer\UAS alone.

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

eag1/Rat\CamKII-IAla.hs individuals also fail to court.

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.

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.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
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Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments

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

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
References (60)