FlyBase Allele Report: Dmel\Sh[14]

General Information

Symbol

Dmel\Sh¹⁴

Species

D. melanogaster

Name

FlyBase ID

FBal0015554

Feature type

allele

Associated gene

Dmel\Sh

Associated Insertion(s)

Carried in Construct

Also Known As

sh^KS133, Sh¹³³

Key Links

Genomic Maps

JBrowse

Allele class

amorphic allele - genetic evidence

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Hardie et al., 1991, Mallart et al., 1991)

Mutagen

ethyl methanesulfonate

(de la Pompa, 1994, Balakrishnan and Rodrigues, 1991, Mallart et al., 1991, Gautam and Tanouye, 1990, Kamb et al., 1987)

Progenitor genotype

Cytology

Polytene chromosomes normal.

(Ferrus et al., 1990)

Description

A missense mutation in the core region of the Sh¹⁴ protein results in nonfunctional Sh channels.

(Vahasoyrinki et al., 2006)

Missense mutation between the S5 and S6 transmembrane-spanning domains.

(Martinez-Padron and Ferrus, 1997)

Missense mutation in the core region.

(Hevers and Hardie, 1995)

Missense mutation in the region between the S5 and S6 transmembrane-spanning domains.

(Tsunoda and Salkoff, 1995)

Missense mutation in the region connecting the proposed transmembrane segments S5 and S6 of the Sh K⁺ channel proteins.

(de la Pompa, 1994)

A missense mutation in the core region.

(Hardie et al., 1991)

Mutation in the V region of the Sh locus.

(Ferrus et al., 1990)

Nucleotide substitution T to A in exon 15. This corresponds to an amino acid change from Val to Asp in the bend region connecting the proposed membrane spanning segments S5 and S6. The Sh¹⁴ mutation is 27bp from the position of the Sh⁷ mutation.

(Lichtinghagen et al., 1990)

Point mutation.

(Kamb et al., 1987)

sequenced by Lichtinghagen et al., 1990 val⁴¹³ to asp; relative to the deduced H37 protein (Kamb, Tseng-Crank and Tanouye, 1988).

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

X:17,945,237..17,945,237 [-]

Nucleotide change:

T17945237A

Reported nucleotide change:

T?A

Amino acid change:

Reported amino acid change:

V429D

(Lichtinghagen et al., 1990)

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, Ganetzky and Wu, 1983)

CEA with eag¹

(Fergestad et al., 2006)

Modifiers Based on Experimental Evidence ( 1 )

Disease

Interaction

References

DOES NOT ameliorate 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

abnormal behavior

(Circelli et al., 2005, Hurd et al., 1996, Ferrus et al., 1990, Gisselmann et al., 1989)

abnormal behavior | dominant

(Stern et al., 1990, Kamb et al., 1987, Ganetzky and Wu, 1982)

abnormal behavior | recessive

(Stern and Ganetzky, 1992)

abnormal chemosensory behavior

(Walcourt et al., 2001)

abnormal neurophysiology

(Cardnell et al., 2006, Vahasoyrinki et al., 2006, Niven et al., 2003, Kuebler et al., 2001, Broadie and Bate, 1993, Broadie and Bate, 1993, Engel and Wu, 1992, Gho and Ganetzky, 1992, Mallart et al., 1991, Ferrus et al., 1990, Ganetzky and Wu, 1983, Ganetzky and Wu, 1982)

abnormal neurophysiology | first instar larval stage

(Wolfram et al., 2012)

abnormal taste perception | recessive

(Balakrishnan and Rodrigues, 1991)

chemical sensitive

(Madhavan et al., 2000)

chemical sensitive | recessive

(Leibovitch et al., 1995)

increased rate of movement

(Mosca et al., 2005, Huang and Stern, 2002, Torroja et al., 1999)

increased rate of movement | dominant

(Cardnell et al., 2006)

uncoordinated

(Mosca et al., 2005, Ganetzky and Wu, 1982)

viable

(Schmidt et al., 2000)

Phenotype Manifest In

Detailed Description

Statement

Reference

Whole cell patch-clamp recordings of dissociated ommatidia from Sh¹⁴ flies show a similar leftward shift of the I/V curve in response to green light stimulation as do recordings of wild-type dissociated ommatidia.

(Krause et al., 2008)

Heterozygous flies show a rapid leg-shaking phenotype when under ether anesthesia.

At low Ca²⁺ levels (0.1mM), the excitatory junctional potential (ejp) elicited in the muscle at the neuromuscular junction has increased amplitude and duration in mutant larvae compared to wild type.

(Cardnell et al., 2006)

Sh¹⁴ flies do not show a significantly shortened lifespan. At day 35, the brains of these flies show intermittent pathology.

(Fergestad et al., 2006)

Electrical current recordings from Sh¹⁴ mutant photoreceptors show the transient K⁺ current is eliminated, but the slowly inactivating current is intact in these mutants.

(Vahasoyrinki et al., 2006)

Mutant flies exhibit a decrease in the daily sleep amount. This is mainly due to a decrease in the duration of sleep episodes rather than in their number. This phenotype is very sensitive to background modifiers.

(Circelli et al., 2005)

Mutant muscles (ventral lateral longitudinal fiber 6 of segments A2 and A3 have been tested) lack the prominent A-type inactivating outward K⁺ current. Dissociated mushroom body intrinsic neurons do not show a dramatic modification of the whole-cell outward K⁺ current profile or a significant decrease in the current density compared to wild type. Two neuronal populations are present in preparations of wild-type dissociated mushroom body intrinsic neurons; a major population (approximately 72%) having half-inactivation voltages of approximately -78mV, and a minor one having more depolarised half-inactivation voltage values. This second population is absent in preparations of Sh¹⁴ dissociated mushroom body intrinsic neurons.

(Gasque et al., 2005)

Mutant adults exhibit both leg shaking and wing scissoring under ether anaesthetization. This behaviour persists in severed legs.

(Mosca et al., 2005)

Sh¹⁴ photoreceptors are grossly morphology normal. Sh¹⁴ photoreceptors are unable to follow sequences of rapid transients, unlike wild-type receptors. For example, light intensity fluctuations of increasing intensity are encoded by increasingly frequent responses in the wild-type photoreceptor, while Sh¹⁴ responses approach a plateau of depolarisations at lower stimulus levels, compressing their responses to bright inputs. Mutant photoreceptors produce large, fast voltage responses to large light intensity increases after dim periods, which are reduced in wild-type photoreceptors. During sustained periods of bright light Sh¹⁴ receptors produce smaller responses than wild-type. Additionally, Sh¹⁴ voltage responses repolarise more rapidly than wild-type voltage responses.

Voltage responses of Sh¹⁴ photoreceptors to naturalistic stimuli are altered compared to wild-type. In particular, many of the transient responses to naturalistic stimuli in Sh¹⁴ are distorted, and the spread of the signal over the available voltage range is reduced in Sh¹⁴ photoreceptors. Sh¹⁴ photoreceptors have large-amplitude, shorter time-to-peak, and shorter half-width linear impulse responses than wild-type.

(Niven et al., 2004)

When presented with sequences of dynamically modulated light with a mean contrast of 0.32, close to that of natural sceneries, over the range of intensities to which photoreceptors are normally exposed, the light induced current, quantum efficiency and macroscopic kinetics are unaffected in Sh¹⁴ photoreceptors. The photoreceptor signal response in reduced in mutant animals, at all background intensities. Mutant flies also have reduced information capacity of photoreceptors at all but the dimmest light levels. The information loss is greatest over the lower frequency range of the spectrum (1-50Hz). Under light adapted conditions the N(f) of mutant photoreceptors are similar to wild-type. Mutant photoreceptor show a reduced contrast gain and broadened bandwidth with increasing mean light intensity. Sh¹⁴ responses contain more high-frequency signals. Mutant photoreceptors have reduced resistances compared to wild-type. Current pulse experiments show that the steady-state conductance of mutant photoreceptors behave as would be expected of a wild-type membrane without Sh, with no further voltage-dependent conductances.

(Niven et al., 2003)

Sh¹⁴ 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 is increased in mutant flies compared to controls; seizures cannot be evoked with the standard 300ms high-frequency stimuli at 100V, but can be evoked using 400ms high-frequency stimuli. Under these conditions, the seizure threshold of the mutant flies is 83.8 +/- 12.8 V.

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 giant fiber following frequency (the maximum stimulation frequency that the giant fiber pathway can reliably follow) is greatly reduced compared to wild type in mutant animals.

(Kuebler et al., 2001)

Homozygous Sh¹⁴ females exhibit a marked increase in sensitivity to halothane in an electrophysiologically monitored escape response. Specifically, halothane EC[[50]] is increased in Sh¹⁴ stocks by 85% over that in wild-type control females. Heterozygous Sh¹⁴ females exhibit a halothane potency that is intermediate between the homozygous mutant and controls. Male Sh⁹ mutants produce a modest increase in EC[[50]] (35% compared to Canton-S flies).

(Walcourt 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)

Mutant flies show an increased sensitivity to halothane in an inebriometer assay compared to control flies, having a higher Response Index of 0.85 +/- 0.09 after 12 minutes of exposure to halothane.

(Madhavan et al., 2000)

I_A and I_K currents are present in cell cultures of midline neurons prepared from Sh¹⁴ mutants.

(Schmidt et al., 2000)

Sh¹⁴ flies treated with sodium valproate (NaVP) show a reduction in body weight, as is seen in wild-type flies. Treatment of Sh¹⁴ flies with NaVP causes an increase in mortality as is seen in wild-type flies.

(Sharma and Kumar, 1999)

slo⁴ partially suppresses the synaptic transmission defects (eliminates the repetitive firing of motor axons).

(Warbington et al., 1996)

Homozygotes show increased sensitivity to halothane, chloroform and trichloroethylene in an inebriometer assay (an assay of geotactic and postural behaviour) compared to wild-type flies. Decapitated flies lose the halothane sensitive phenotype.

(Leibovitch et al., 1995)

More sensitive than the wild-type to the knock-down effect of acute γ-irradiation.

(Megumi et al., 1995)

The delivery of an electrical buzz (50-400 msec) to the brain has no significant effect on Sh¹⁴ mutant flies.

(Pavlidis and Tanouye, 1995)

Two-electrode voltage clamp technique is used to measure end-plate currents in larval neuromuscular junctions. Currents are four fold larger than wild type, lack post-tetanic potentiation (PTP) but could undergo facilitation. PTPs could be restored by addition of Cd²⁺.

(Delgado et al., 1994)

Vigorous and continuous vibration of all appendages. Double mutant combinations with tta¹ show slight suppression of the Sh phenotype. Sh phenotype is enhanced by the presence of one extra copy of tta.

(de la Pompa, 1994)

Completely removes the fast voltage-gated potassium current in muscle during all stages of development (FBrf0043054). Muscles show abnormal transmission characterised by increased transmitter release and prolonged excitatory junction potentials (EJPs) (FBrf0043046). 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, Sh¹⁴ double mutants have normal grooming behavior.

(Phillis et al., 1993)

Flies show leg-shaking under anaesthesia. The action potential of the dorsal longitudinal muscle often appears abnormal in Sh¹⁴ mutants and Sh¹⁴ eag¹ double mutants. Increases the refractory period and lowers the following frequency of the giant fibre response of the dorsal longitudinal muscle pathway and of the tergotrochanteral muscle pathway. eag¹ Sh¹⁴ double mutant flies show spontaneous activity of the dorsal longitudinal and dorsoventral indirect flight muscles when at rest. 86% of eag¹ Sh¹⁴ flies have a wings-down phenotype.

(Engel and Wu, 1992)

Sh¹⁴ and DAP (3,4-diaminopyridine) cause the same increase in synaptic delay and the same reduction in the slope of onset phase of electrotonically evoked synaptic current in slo mutant third instar larvae.

(Gho and Ganetzky, 1992)

Leg shaking while under ether anaesthesia.

(Stern 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)

Heterozygotes show ether induced leg shaking. Hemizygous males show a reduced preference for sucrose compared to wild-type in feeding preference tests, probably due to a shift in the threshold of detection. Flies show no attraction to 100mM NaCl and an increased tolerance to 0.5M NaCl and 0.2M KCl compared to wild-type. The increased tolerance to 0.5M NaCl and 0.2M KCl is due to an increase in the threshold of repulsion. The firing patterns of the labellar chemosensory neurons in response to sucrose, NaCl and KCl are normal.

(Balakrishnan and Rodrigues, 1991)

Muscle fibres and photoreceptors have no detectable I_A (rapidly inactivating A current).

(Hardie et al., 1991)

Presynaptic action potential decay time is considerably prolonged in Sh¹⁴ third instar neuromuscular junctions compared to wild-type.

(Mallart et al., 1991)

The leg shaking phenotype of Sh¹⁴ is enhanced by Dp(1;4)r⁺l. 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.

(Budnik et al., 1990)

Flies manifest chronic vibration of their appendages as well as abnormal action potentials.

(Ferrus et al., 1990)

I_A is completely eliminated in homozygous third larval instar muscles. I_A is much lower than predicted by simple gene-dosage dependence in Sh¹⁴/+, Sh¹⁴/Sh²¹, Sh¹⁴/Sh⁹ and Sh¹⁴/Sh⁵ flies.

(Haugland and Wu, 1990)

The voltage-activated fast K⁺ current (I_A) is eliminated in larval muscle fibres.

(Singh and Wu, 1990)

Heterozygous flies show rapid-leg shaking under ether anesthesia.

(Stern et al., 1990)

A-type current is completely absent.

(Gisselmann et al., 1989)

Excitatory junction potentials are prolonged even at very low external Ca²⁺ concentrations. eag¹ interacts synergistically with Sh¹⁴ in double mutants to produce extremely prolonged neuromuscular transmission and spontaneous firing of the motor axons.

(Ganetzky and Wu, 1983)

Ether-dependent leg shaking and wing scissoring. Chloroform, ethyl acetate and carbon dioxide etherization does not elicit shaking behavior, though nitrogen and triethylkamine etherization does. Unetherized, older flies show uncoordinated walking behavior, and stand quivering on the bottom of the culture bottle. In the larval neuromuscular junction preparation, repetetive firing of the motor axons is associated with a prolonged release of neurotransmitter at the nmj producing a prolonged, large ejp.

(Ganetzky and Wu, 1982)

abnormal leg shaking under ether anesthesia; abnormal A-type potassium currents in larval muscle and/or pupal flight muscle; abnormal action potentials in the adult cervical giant fiber; abnormal synaptic transmission at the larval neuromuscular junction and multiple firing of larval motoneurons.

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Sh¹⁴ has abnormal neurophysiology phenotype, enhanceable by Shab³

(Vahasoyrinki et al., 2006)

NOT Enhanced by

Statement

Reference

Sh¹⁴ has abnormal neurophysiology | first instar larval stage | recessive phenotype, non-enhanceable by tup^{UAS.Tag:Dam,Tag:MYC}/Scer\GAL4^eve.RN2O

(Wolfram et al., 2012)

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

(Fergestad et al., 2006)

Suppressed by

Statement

Reference

Sh¹⁴ has abnormal neurophysiology phenotype, suppressible by eag^G297E

(Cardnell et al., 2006)

Sh¹⁴ has abnormal neurophysiology phenotype, suppressible by eag^VV

(Cardnell et al., 2006)

Sh¹⁴ has increased rate of movement | dominant phenotype, suppressible by eag^G297E

(Cardnell et al., 2006)

Sh¹⁴ has abnormal neurophysiology phenotype, suppressible by eag^G297E/eag[+]

(Cardnell et al., 2006)

Sh¹⁴ has abnormal neurophysiology phenotype, suppressible by eag^G297E/eag^G297E

(Cardnell et al., 2006)

Sh¹⁴ has viable phenotype, suppressible by Shab³

(Vahasoyrinki et al., 2006)

Sh¹⁴ has abnormal behavior phenotype, suppressible by Khc^1ts

(Hurd et al., 1996)

Sh¹⁴ has abnormal behavior phenotype, suppressible by Khc⁶/Khc^BD

(Hurd et al., 1996)

NOT suppressed by

Statement

Reference

Sh¹⁴ has abnormal neurophysiology | recessive | first instar larval stage phenotype, non-suppressible by tup^{UAS.Tag:Dam,Tag:MYC}/Scer\GAL4^eve.RN2O

(Wolfram et al., 2012)

Enhancer of

Statement

Reference

Sh¹⁴ is an enhancer of abnormal neurophysiology phenotype of Shab³

(Vahasoyrinki et al., 2006)

Sh¹⁴ is an enhancer of partially lethal | male phenotype of Scer\GAL4^elav-C155, Shaw^{tr.UAS.Tag:FLAG}

(Hodge et al., 2005)

Sh¹⁴ is an enhancer of visible | adult stage A1 phenotype of Scer\GAL4^elav-C155, Shaw^{tr.UAS.Tag:FLAG}

(Hodge et al., 2005)

Sh¹⁴ is an enhancer of abnormal eclosion phenotype of Scer\GAL4^elav-C155, Shaw^{tr.UAS.Tag:FLAG}

(Hodge et al., 2005)

Sh¹⁴ is an enhancer of lethal | embryonic stage phenotype of Scer\GAL4^C164, Shaw^{RA.UAS.Tag:FLAG}

(Hodge et al., 2005)

Sh¹⁴ is an enhancer of lethal | embryonic stage phenotype of Scer\GAL4^elav-C155, Shaw^{RA.UAS.Tag:FLAG}

(Hodge et al., 2005)

Sh¹⁴ is an enhancer of visible | adult stage A1 phenotype of Scer\GAL4^C164, Shaw^{tr.UAS.Tag:FLAG}

(Hodge et al., 2005)

Sh¹⁴ is an enhancer of abnormal body size | pharate adult stage phenotype of Scer\GAL4^C164, Shaw^{tr.UAS.Tag:FLAG}

(Hodge et al., 2005)

Sh¹⁴ is an enhancer of abnormal eclosion phenotype of Scer\GAL4^C164, Shaw^{tr.UAS.Tag:FLAG}

(Hodge et al., 2005)

NOT Enhancer of

Statement

Reference

Sh¹⁴/Sh¹⁴ is a non-enhancer of abnormal neurophysiology | first instar larval stage | recessive phenotype of Scer\GAL4^eve.RN2O, tup^{UAS.Tag:Dam,Tag:MYC}

(Wolfram et al., 2012)

Sh¹⁴/Sh[+] is a non-enhancer of short lived | dominant phenotype of Atpα^DTS1

(Fergestad et al., 2006)

Suppressor of

Statement

Reference

Sh¹⁴/Sh¹⁴ is a suppressor of abnormal neurophysiology | recessive | first instar larval stage phenotype of tup^isl-1

(Wolfram et al., 2012)

Sh¹⁴ is a suppressor of viable phenotype of Shab³

(Vahasoyrinki et al., 2006)

Sh¹⁴ is a suppressor | partially of abnormal neurophysiology phenotype of jus^iso6.10

(Kuebler et al., 2001)

NOT Suppressor of

Statement

Reference

Sh¹⁴ is a non-suppressor of abnormal neuroanatomy | third instar larval stage phenotype of Scer\GAL4^insc-Mz1407, dpn^UAS.cWa

(Huang et al., 2015)

Sh¹⁴ is a non-suppressor 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

Sh¹⁴, tup^isl-1 has lethal - all die during embryonic stage phenotype

(Wolfram et al., 2012)

Sh¹⁴, eag¹ has short lived phenotype

(Fergestad et al., 2006)

Sh¹⁴, Shab³ has sterile phenotype

(Vahasoyrinki et al., 2006)

Sh¹⁴, smi26D¹ has abnormal locomotor behavior | dominant | female phenotype

(Anholt et al., 2003)

Sh¹⁴, smi26D¹ has abnormal smell perception | dominant | female phenotype

(Anholt et al., 2003)

Sh¹⁴, smi26D¹ has abnormal smell perception | dominant | male phenotype

(Anholt et al., 2003)

Sh¹⁴, smi26D¹/smi26D[+] has abnormal locomotor behavior | dominant | female phenotype

(Anholt et al., 2003)

Sh¹⁴, smi26D¹/smi26D[+] has abnormal smell perception | dominant | female phenotype

(Anholt et al., 2003)

Sh¹⁴, smi26D¹/smi26D[+] has abnormal smell perception | dominant | male phenotype

(Anholt et al., 2003)

Sh¹⁴, ine¹ has visible phenotype

(Huang and Stern, 2002)

Phenotype Manifest In

Enhanced by

Statement

Reference

Sh¹⁴ has photoreceptor phenotype, enhanceable by Shab³

(Vahasoyrinki et al., 2006)

NOT Enhanced by

Statement

Reference

Sh¹⁴ has embryonic/larval motor neuron | first instar larval stage phenotype, non-enhanceable by tup^{UAS.Tag:Dam,Tag:MYC}/Scer\GAL4^eve.RN2O

(Wolfram et al., 2012)

Suppressed by

Statement

Reference

Sh¹⁴ has leg phenotype, suppressible by eag^G297E

(Cardnell et al., 2006)

Sh¹⁴ has embryonic/larval neuromuscular junction phenotype, suppressible by eag^G297E/eag[+]

(Cardnell et al., 2006)

Sh¹⁴ has embryonic/larval neuromuscular junction phenotype, suppressible by eag^G297E/eag^G297E

(Cardnell et al., 2006)

Sh¹⁴ has phenotype, suppressible by Scer\GAL4^Appl.G1a/Appl^UAS.cTa

(Torroja et al., 1999)

Sh¹⁴ has phenotype, suppressible by Scer\GAL4^elav-C155/Appl^UAS.cTa

(Torroja et al., 1999)

Sh¹⁴ has phenotype, suppressible by Khc⁴

(Hurd et al., 1996)

Sh¹⁴ has phenotype, suppressible by Khc⁵

(Hurd et al., 1996)

Sh¹⁴ has leg phenotype, suppressible by Khc^1ts

(Hurd et al., 1996)

Sh¹⁴ has leg phenotype, suppressible by Khc⁶/Khc^BD

(Hurd et al., 1996)

Sh¹⁴ has phenotype, suppressible by para¹⁰³

(Stern et al., 1990)

Sh¹⁴ has phenotype, suppressible by para⁶⁰

(Stern et al., 1990)

Sh¹⁴ has phenotype, suppressible by para⁷⁴

(Stern et al., 1990)

NOT suppressed by

Statement

Reference

Sh¹⁴ has embryonic/larval motor neuron | first instar larval stage phenotype, non-suppressible by tup^{UAS.Tag:Dam,Tag:MYC}/Scer\GAL4^eve.RN2O

(Wolfram et al., 2012)

Enhancer of

Statement

Reference

Sh¹⁴ is an enhancer of photoreceptor phenotype of Shab³

(Vahasoyrinki et al., 2006)

Sh¹⁴ is an enhancer of wing phenotype of Scer\GAL4^elav-C155, Shaw^{tr.UAS.Tag:FLAG}

(Hodge et al., 2005)

Sh¹⁴ is an enhancer of adult cuticle phenotype of Scer\GAL4^elav-C155, Shaw^{tr.UAS.Tag:FLAG}

(Hodge et al., 2005)

Sh¹⁴ is an enhancer of wing phenotype of Scer\GAL4^C164, Shaw^{tr.UAS.Tag:FLAG}

(Hodge et al., 2005)

Sh¹⁴ is an enhancer of adult cuticle phenotype of Scer\GAL4^C164, Shaw^{tr.UAS.Tag:FLAG}

(Hodge et al., 2005)

NOT Enhancer of

Statement

Reference

Sh¹⁴/Sh¹⁴ is a non-enhancer of embryonic/larval motor neuron | first instar larval stage phenotype of Scer\GAL4^eve.RN2O, tup^{UAS.Tag:Dam,Tag:MYC}

(Wolfram et al., 2012)

Suppressor of

Statement

Reference

Sh¹⁴/Sh¹⁴ is a suppressor of embryonic/larval motor neuron | first instar larval stage phenotype of tup^isl-1

(Wolfram et al., 2012)

NOT Suppressor of

Statement

Reference

Sh¹⁴ is a non-suppressor of type I neuroblast | third instar larval stage phenotype of Scer\GAL4^insc-Mz1407, dpn^UAS.cWa

(Huang et al., 2015)

Sh¹⁴ is a non-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

Sh¹⁴, ine¹ has wing phenotype

(Huang and Stern, 2002)

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

(Torroja et al., 1999)

Dp(1;4)r⁺l, Sh¹⁴ has wing phenotype

(Stern et al., 1990)

Dp(1;4)r⁺l, Sh¹⁴ has adult thorax | dorsal phenotype

(Stern et al., 1990)

Additional Comments

Genetic Interactions

Statement

Reference

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)

The ether-induced leg shaking of Sh¹⁴ mutants is suppressed by both eag^G297E and eag^VV.

(Cardnell et al., 2006)

eag^G297E suppresses the mutant excitatory junctional potential (ejp) phenotype that is seen at low Ca²⁺ levels (0.1mM) in Sh¹⁴ larvae in a dosage dependent manner; eag^G297E/+ results in a moderate decrease in the ejp amplitude, but not ejp duration, while eag^G297E/eag^G297E significantly decreases both ejp amplitude and duration. This suppression requires extracellular Mg²⁺.

The average amplitude of the excitatory junctional current (ejc) at the neuromuscular junction is significantly smaller in eag^G297E Sh¹⁴ animals than in eag⁺ Sh¹⁴ animals. The average amplitude of the spontaneous miniature excitatory junctional potential (mejp) is almost identical in eag^G297E Sh¹⁴ and eag⁺ Sh¹⁴ animals.

(Cardnell et al., 2006)

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. Sh¹⁴/+; Atpα^DTS1/+ double mutants have a similar lifespan to Atpα^DTS1/+ single mutants.

(Fergestad et al., 2006)

Sh¹⁴; Shab³ double mutants are poorly viable and infertile.

Examination of Shab³ photoreceptor whole-cell currents reveals that the steady-state current is at least two-times greater than in Sh¹⁴; Shab³ double mutants.

(Vahasoyrinki et al., 2006)

Adults overexpressing Shaw^{tr.Scer\UAS.T:Zzzz\FLAG} with either Scer\GAL4^elav-C155 or Scer\GAL4^C164, in combination with Sh¹⁴, show an ether-induced shaking phenotype. Some adults show a phenotype with unfurled wings and softened or abnormally tanned cuticle. Some small pupae fail to eclose.

Males and females expressing Shaw^{tr.Scer\UAS.T:Zzzz\FLAG} with Scer\GAL4^C164, in combination with Sh¹⁴, show reduced body weight when compared to controls.

(Hodge et al., 2005)

Expression of ine^RA.Scer\UAS driven by either Scer\GAL4^Gli-rL82 or Scer\GAL4^elav.PLu fully suppresses the downturned wings phenotype of Sh¹⁴ ine¹, along with the increased rate of onset of long-term facilitation phenotype. These flies also require even more repetitive nerve stimulation compared to wild-type for the onset of long-term facilitation. Expression of ine^RA.Scer\UAS in larval stage neurons, under the regulation of Scer\GAL4^elav.PLu partially suppresses the long-term facilitation phenotype. Expression of ine^RA.Scer\UAS driven by Scer\GAL4^MZ1580 in the glia, results in 94% rescue of the Sh¹⁴ ine¹ downturned wing phenotype. The Sh¹⁴ hyperexcitability phenotype, such as leg-shaking, can be suppressed by expression of ine^RA.Scer\UAS under the control of Scer\GAL4^MZ1580. Suppression of the downturned wing phenotype of Sh¹⁴ ine¹ occurs upon the induction of ine^hs.P1 by a single heat pulse immediately before eclosion. Induction of ine^hs.P1 after eclosion did not rescue the downturned wings phenotype.

Expression of ine^RA.Scer\UAS driven by either Scer\GAL4^Gli-rL82 or Scer\GAL4^MZ1580 fully suppresses the downturned wings phenotype of Sh¹⁴ ine¹.

The Sh¹⁴ hyperexcitability phenotype, such as leg-shaking, can be suppressed by expression of ine^RA.Scer\UAS under the control of Scer\GAL4^MZ1580.

Suppression of the downturned wing phenotype of Sh¹⁴ ine¹ occurs upon the induction of ine^hs.P1 by a single heat pulse immediately before eclosion. Induction of ine^hs.P1 after eclosion does not rescue the downturned wings phenotype.

(Huang and Stern, 2002)

Sh¹⁴ partially suppresses the reduced seizure threshold of sda^iso6.10 flies following high-frequency electrical stimuli.

The threshold for activation of the giant fiber in sda^iso6.10 Sh¹⁴ animals following single stimulus pulses (0.2ms duration, 0.5Hz) is not significantly different from that of wild type.

(Kuebler et al., 2001)

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 Sh¹⁴ mutants, and this phenotype is reversed by addition of one copy of Khc^+t7.5.

(Hurd et al., 1996)

The Sh¹⁴/+ leg shaking phenotype is suppressed by para⁶⁰, para⁶³, para⁷⁴, para¹⁰³ and para¹⁴¹. Sh¹⁴; Dp(1;4)r⁺l flies have downturned wings and an indentation of the dorsal thorax. The increase in membrane excitability caused by Sh¹⁴ is partially suppressed by para⁶⁰. The wing and thorax phenotype seen in Sh¹⁴; Dp(1;4)r⁺l flies is caused by the extra dosage of para⁺, since para^lk5 Sh¹⁴ ; Dp(1;4)r⁺l flies, in which the para⁺ dosage is restored to normal, have normal wings and thorax.

(Stern et al., 1990)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Comments

Images (0)

Mutant

Wild-type

Stocks (8)

Bloomington

4741

Df(1)B25, Sh¹⁴/FM6

4752

Ab(1)os^s, ff¹ Sh¹⁴ upd1^os-s upd3^os-s/FM6

6350

sc^e rut¹ f⁵ Sh¹⁴/C(1)DX, y¹ w¹ f¹

Kyoto

107100

Sh¹⁴

107853

Df(1)B25, Sh¹⁴/FM6

108747

sc^e rut¹ f⁵ Sh¹⁴/C(1)DX, y¹ f¹

107859

Ab(1)os^s, ff¹ Sh¹⁴ upd1^os-s upd3^os-s/FM6

102048

sc^e rut¹ f⁵ Sh¹⁴ / C(1)DX, y¹ f¹

Notes on Origin

Discoverer

Searcy.

Comments

Both whole fly and larval neuromuscular junction phenotypes are suppressed by mle^nap-ts1, even at permissive temperatures. Shaking and suppressed phenotypes are evident in severed legs as well as in the whole organism.

(Ganetzky and Wu, 1982)

Mutation site is identical to that of Sh⁷ and Sh⁵.

(Kamb et al., 1987)

Allelic series of Sh defects: Sh⁷ > Sh¹⁴ > Sh¹⁶ > Sh⁵ > Sh⁹.

(Gisselmann et al., 1989)

Sh¹⁴ and Sh⁵ are not separable by recombination so are suggested to be closely linked point mutations.

(Ferrus et al., 1990)

The physiological properties and role in membrane excitability of I_A, the Ca²⁺-activated fast K⁺ current (I_CF) and the voltage-activated delayed K⁺ current (I_K) have been investigated using Sh¹⁴ and slo¹ mutant larval muscle fibres and quinidine (which blocks I_K). Current-clamp recordings from wild-type, Sh¹⁴, slo¹ and Sh¹⁴ slo¹ double mutant larval muscle fibres suggest that I_CF plays a stronger role than I_A in repolarisation of the larval muscle membrane.

(Singh and Wu, 1990)

The severity of the sucrose preference defect shows the following order: Sh⁸ > Sh⁵ = Sh⁷ > Sh²⁵ > T(1;Y)V7 > Sh¹⁴. The degree of tolerance to 0.5M NaCl shows the order: Sh⁸ > Sh⁷ = Sh⁵ > T(1;Y)V7 = Sh²⁵ > Sh¹⁴. The degree of tolerance to 0.2M KCl shows the order: Sh⁸ = Sh⁷ = Sh¹⁴ > T(1;Y)V7 > Sh⁵.

(Balakrishnan and Rodrigues, 1991)

In homozygotes postsynaptic GluRIIA expression is unaffected. eag¹ Sh¹⁴ double mutants significantly reduce postsynaptic expression of GluRIIA by the end of embryogenesis.

(Broadie and Bate, 1993)

Eliminate the I_A current.

(Broadie and Bate, 1993)

Electrophysiological analysis reveals that action potentials have a long repolarization delay.

(de la Pompa, 1994)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (11)

Reported As

Symbol Synonym

KS133

(Hosler et al., 2000)

Sh133

(Lee and Wu, 2002)

Sh¹³³

(Ruan et al., 2017, Iyengar and Wu, 2014, Fergestad et al., 2010, Ataman et al., 2008, Cardnell et al., 2006, Fergestad et al., 2006, Ueda and Wu, 2006, Circelli et al., 2005, Huang et al., 2002, Engel and Wu, 1998, Phillis et al., 1993, Zhong et al., 1992)

Sh¹⁴

(Ho and Treisman, 2020, Davis et al., 2018, Huang et al., 2015, Wolfram et al., 2012, Koh et al., 2008, Niven et al., 2004, Schmidt et al., 2000)

Sh^KS133

(Harrigan et al., 2020, Ping et al., 2011, Hodge et al., 2005, Niven et al., 2003, Huang and Stern, 2002, Kuebler et al., 2001, Walcourt et al., 2001, Brenner et al., 2000, Madhavan et al., 2000, Torroja et al., 1999, Torroja et al., 1999, Engel and Wu, 1998, Peretz et al., 1998, Kraliz and Singh, 1997, Lin and Nash, 1997, Martinez-Padron and Ferrus, 1997, Hurd et al., 1996, Warbington et al., 1996, Hevers and Hardie, 1995, Leibovitch et al., 1995, Lin and Nash, 1995, Pavlidis and Tanouye, 1995, Tsunoda and Salkoff, 1995, Yokokura et al., 1995, Chopra and Singh, 1994, de la Pompa, 1994, Delgado et al., 1994, Broadie and Bate, 1993, Broadie and Bate, 1993, Engel and Wu, 1992, Stern and Ganetzky, 1992, Balakrishnan and Rodrigues, 1991, Hardie, 1991, Hardie, 1991, Hardie et al., 1991, Mallart et al., 1991, Budnik et al., 1990, Ferrus et al., 1990, Gautam and Tanouye, 1990, Haugland and Wu, 1990, Komatsu et al., 1990, Lichtinghagen et al., 1990, Singh and Wu, 1990, Stern et al., 1990, Gisselmann et al., 1989, Baumann et al., 1987, Kamb et al., 1987, Ganetzky and Wu, 1983, Ganetzky and Wu, 1982)

Sh^ks133

(Byers et al., 2021, Mir and Krishnan, 1995)

Sh[133]

(Cardnell et al., 2006)

sh¹³³

(Hosler et al., 2000)

sh¹⁴

(Mozer and Sandstrom, 2012)

sh^KS133

(Krause et al., 2008, Gasque et al., 2005)

Name Synonyms

Shaker14

(Vahasoyrinki et al., 2006)

Secondary FlyBase IDs

References (87)

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