Allele Dmel\Sh¹⁴

General Information
Symbol	Dmel\Sh¹⁴	Species	D. melanogaster
Name		FlyBase ID	FBal0015554
Feature type	allele	Associated gene	Dmel\Sh
Also Known As	sh^KS133, Sh¹³³

Allele class	amorphic allele - genetic evidence
Mutagen	ethyl methanesulfonate
Recent Updates
Description	What does this section display? This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms). What does this section not display? This section does not currently display links that were removed or gene model changes.
Update Feed	Click the icon below to subscribe to this FlyBase record and receive updates automatically through your feed reader.
FB2013_03
FB2013_02
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Nature of the Allele
Allele class	amorphic allele - genetic evidence (Mallart et al., 1991, Hardie et al., 1991)
Mutagen	ethyl methanesulfonate (Kamb et al., 1987, Gautam and Tanouye, 1990, Mallart et al., 1991, Balakrishnan and Rodrigues, 1991, de la Pompa, 1994)
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 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).
Cytology	Polytene chromosomes normal. (Ferrus et al., 1990)
Phenotypic Data
Phenotypic Class
	behavior defective (Gisselmann et al., 1989, Hurd et al., 1996, Ferrus et al., 1990, Circelli et al., 2005) behavior defective \| dominant (Kamb et al., 1987, Stern et al., 1990, Ganetzky and Wu, 1982) behavior defective \| recessive (Stern and Ganetzky, 1992) chemical sensitive (Madhavan et al., 2000) chemical sensitive \| recessive (Leibovitch et al., 1995) hyperactive (Mosca et al., 2005, Torroja et al., 1999, Huang and Stern, 2002) hyperactive \| dominant (Cardnell et al., 2006) neurophysiology defective (Engel and Wu, 1992, Niven et al., 2003, Broadie and Bate, 1993, Mallart et al., 1991, Ganetzky and Wu, 1983, Ganetzky and Wu, 1982, Broadie and Bate, 1993, Ferrus et al., 1990, Gho and Ganetzky, 1992, Cardnell et al., 2006, Vahasoyrinki et al., 2006, Kuebler et al., 2001) taste perception defective \| recessive (Balakrishnan and Rodrigues, 1991) uncoordinated (Mosca et al., 2005, Ganetzky and Wu, 1982) viable (Schmidt et al., 2000)
Phenotype Manifest In
	embryonic/larval neuromuscular junction (Cardnell et al., 2006) end plate (Delgado et al., 1994) giant fiber neuron (Kuebler et al., 2001) leg (Hurd et al., 1996, Cardnell et al., 2006) muscle fiber (Hardie et al., 1991) muscle fiber \| larval stage (Singh and Wu, 1990) neuromuscular junction (Broadie and Bate, 1993) photoreceptor (Vahasoyrinki et al., 2006) photoreceptor cell (Hardie et al., 1991) synapse (Broadie and Bate, 1993)
Detailed Description
	Statement Reference Whole cell patch-clamp recordings of dissociated ommatidia from Sh[14] 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) 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) 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) 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) 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) 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 the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement Reference Sh¹⁴ has neurophysiology defective phenotype, enhanceable by Shab³ (Vahasoyrinki et al., 2006)
Suppressed by
Statement Reference Sh¹⁴ has behavior defective phenotype, suppressible by Khc^1ts (Hurd et al., 1996) Sh¹⁴ has behavior defective phenotype, suppressible by Khc⁶/Khc^BD (Hurd et al., 1996) Sh¹⁴ has hyperactive \| dominant phenotype, suppressible by eag^G297E (Cardnell et al., 2006) Sh¹⁴ has neurophysiology defective phenotype, suppressible \| partially by eag^G297E/eag[+] (Cardnell et al., 2006) Sh¹⁴ has neurophysiology defective phenotype, suppressible \| partially by eag^G297E/eag^G297E (Cardnell et al., 2006) Sh¹⁴ has neurophysiology defective phenotype, suppressible by eag^G297E (Cardnell et al., 2006) Sh¹⁴ has neurophysiology defective phenotype, suppressible by eag^VV (Cardnell et al., 2006) Sh¹⁴ has viable phenotype, suppressible by Shab³ (Vahasoyrinki et al., 2006)
Enhancer of
Statement Reference Sh¹⁴ is an enhancer of body size defective \| pharate adult stage phenotype of Scer\GAL4^C164, Shaw^{tr.Scer\UAS.T:Zzzz\FLAG} (Hodge et al., 2005) Sh¹⁴ is an enhancer of eclosion defective phenotype of Scer\GAL4^C164, Shaw^{tr.Scer\UAS.T:Zzzz\FLAG} (Hodge et al., 2005) Sh¹⁴ is an enhancer of eclosion defective phenotype of Scer\GAL4^elav-C155, Shaw^{tr.Scer\UAS.T:Zzzz\FLAG} (Hodge et al., 2005) Sh¹⁴ is an enhancer of lethal \| embryonic stage phenotype of Scer\GAL4^C164, Shaw^{RA.Scer\UAS.T:Zzzz\FLAG} (Hodge et al., 2005) Sh¹⁴ is an enhancer of lethal \| embryonic stage phenotype of Scer\GAL4^elav-C155, Shaw^{RA.Scer\UAS.T:Zzzz\FLAG} (Hodge et al., 2005) Sh¹⁴ is an enhancer of lethal \| male \| partially phenotype of Scer\GAL4^elav-C155, Shaw^{tr.Scer\UAS.T:Zzzz\FLAG} (Hodge et al., 2005) Sh¹⁴ is an enhancer of neurophysiology defective phenotype of Shab³ (Vahasoyrinki et al., 2006) Sh¹⁴ is an enhancer of viable \| male \| reduced phenotype of Scer\GAL4^Ccap.PP, Shaw^{RA.Scer\UAS.T:Zzzz\FLAG} (Hodge et al., 2005) Sh¹⁴ is an enhancer of visible \| adult stage A1 phenotype of Scer\GAL4^C164, Shaw^{tr.Scer\UAS.T:Zzzz\FLAG} (Hodge et al., 2005) Sh¹⁴ is an enhancer of visible \| adult stage A1 phenotype of Scer\GAL4^elav-C155, Shaw^{tr.Scer\UAS.T:Zzzz\FLAG} (Hodge et al., 2005)
NOT Enhancer of
Statement Reference Sh¹⁴/Sh[+] is a non-enhancer of short lived \| dominant phenotype of Atpα^DTS1 (Fergestad et al., 2006)
Suppressor of
Statement Reference Sh¹⁴ is a suppressor \| partially of neurophysiology defective phenotype of sda^iso6.10 (Kuebler et al., 2001) Sh¹⁴ is a suppressor of viable phenotype of Shab³ (Vahasoyrinki et al., 2006)
Other
Statement Reference Sh¹⁴, eag¹ has short lived phenotype (Fergestad et al., 2006, Fergestad et al., 2006) Sh¹⁴, ine¹ has visible phenotype (Huang and Stern, 2002) Sh¹⁴, Shab³ has sterile phenotype (Vahasoyrinki et al., 2006, Vahasoyrinki et al., 2006) Sh¹⁴, smi26D¹/smi26D[+] has locomotor behavior defective \| dominant \| female phenotype (Anholt et al., 2003) Sh¹⁴, smi26D¹/smi26D[+] has smell perception defective \| dominant \| female phenotype (Anholt et al., 2003) Sh¹⁴, smi26D¹/smi26D[+] has smell perception defective \| dominant \| male phenotype (Anholt et al., 2003) Sh¹⁴, smi26D¹ has locomotor behavior defective \| dominant \| female phenotype (Anholt et al., 2003) Sh¹⁴, smi26D¹ has smell perception defective \| dominant \| female phenotype (Anholt et al., 2003) Sh¹⁴, smi26D¹ has smell perception defective \| dominant \| male phenotype (Anholt et al., 2003)
Phenotype Manifest In
Enhanced by
Statement Reference Sh¹⁴ has photoreceptor phenotype, enhanceable by Shab³ (Vahasoyrinki et al., 2006)
Suppressed by
Statement Reference Sh¹⁴ has embryonic/larval neuromuscular junction phenotype, suppressible \| partially by eag^G297E/eag[+] (Cardnell et al., 2006) Sh¹⁴ has embryonic/larval neuromuscular junction phenotype, suppressible \| partially by eag^G297E/eag^G297E (Cardnell et al., 2006) Sh¹⁴ has leg phenotype, suppressible by eag^G297E (Cardnell et al., 2006) 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 Khc⁴ (Hurd et al., 1996) Sh¹⁴ has phenotype, suppressible by Khc⁵ (Hurd et al., 1996) Sh¹⁴ has phenotype, suppressible by para⁶⁰ (Stern et al., 1990) Sh¹⁴ has phenotype, suppressible by para⁷⁴ (Stern et al., 1990) Sh¹⁴ has phenotype, suppressible by para¹⁰³ (Stern et al., 1990) Sh¹⁴ has phenotype, suppressible by Scer\GAL4^Appl.G1a/Appl^Scer\UAS.cTa (Torroja et al., 1999) Sh¹⁴ has phenotype, suppressible by Scer\GAL4^elav-C155/Appl^Scer\UAS.cTa (Torroja et al., 1999)
Enhancer of
Statement Reference Sh¹⁴ is an enhancer of adult cuticle phenotype of Scer\GAL4^C164, Shaw^{tr.Scer\UAS.T:Zzzz\FLAG} (Hodge et al., 2005) Sh¹⁴ is an enhancer of adult cuticle phenotype of Scer\GAL4^elav-C155, Shaw^{tr.Scer\UAS.T:Zzzz\FLAG} (Hodge et al., 2005) Sh¹⁴ is an enhancer of photoreceptor phenotype of Shab³ (Vahasoyrinki et al., 2006) Sh¹⁴ is an enhancer of wing phenotype of Scer\GAL4^C164, Shaw^{tr.Scer\UAS.T:Zzzz\FLAG} (Hodge et al., 2005) Sh¹⁴ is an enhancer of wing phenotype of Scer\GAL4^elav-C155, Shaw^{tr.Scer\UAS.T:Zzzz\FLAG} (Hodge et al., 2005)
Other
Statement Reference Appl^sd.Scer\UAS, Scer\GAL4^unspecified, Sh¹⁴, eag¹ has bouton phenotype (Torroja et al., 1999, Torroja et al., 1999, Torroja et al., 1999) Dp(1;4)r⁺l, Sh¹⁴ has adult thorax \| dorsal phenotype (Stern et al., 1990) Dp(1;4)r⁺l, Sh¹⁴ has wing phenotype (Stern et al., 1990) Sh¹⁴, ine¹ has wing phenotype (Huang and Stern, 2002, Huang and Stern, 2002)
Additional Comments
Genetic Interactions
Statement Reference eag[1] Sh[14] 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 Sh[14], 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 Sh[14], 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. (Huang and Stern, 2002) 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) Sh[14] 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] Sh[14] 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 & Rescue Data
Comments
Stocks ( 9 )
Bloomington	3563 Sh¹⁴ 4741 Df(1)B25, Sh¹⁴/FM6 4752 ff¹ Sh¹⁴ os^s/FM6 6350 sc^e rut¹ f⁵ Sh¹⁴/C(1)DX, y¹ w¹ f¹
Kyoto	107100 Sh¹⁴ 107853 Df(1)B25, Sh¹⁴/FM6 107859 ff¹ Sh¹⁴ os^s/FM6 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	Searcy.

Comments
	Electrophysiological analysis reveals that action potentials have a long repolarization delay. (de la Pompa, 1994) 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) 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) 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) Allelic series of Sh defects: Sh⁷ > Sh¹⁴ > Sh¹⁶ > Sh⁵ > Sh⁹. (Gisselmann et al., 1989) Mutation site is identical to that of Sh⁷ and Sh⁵. (Kamb et al., 1987) 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)
External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 11 )
Reported As
Symbol Synonym	KS133 (Hosler et al., 2000) Sh133 (Lee and Wu, 2002) Sh[133] (Cardnell et al., 2006) Sh¹⁴ (Schmidt et al., 2000, Koh et al., 2008) sh¹⁴ (Mozer and Sandstrom, 2012) Sh¹³³ (Fergestad et al., 2006, Circelli et al., 2005, Huang et al., 2002, Engel and Wu, 1998, Phillis et al., 1993, Zhong et al., 1992, Cardnell et al., 2006, Ueda and Wu, 2006, Ataman et al., 2008, Fergestad et al., 2010) sh¹³³ (Hosler et al., 2000) sh^KS133 (Gasque et al., 2005, Krause et al., 2008) Sh^KS133 (Huang and Stern, 2002, Niven et al., 2003, Torroja et al., 1999, Torroja et al., 1999, Peretz et al., 1998, Lin and Nash, 1997, Engel and Wu, 1998, Martinez-Padron and Ferrus, 1997, Kraliz and Singh, 1997, Warbington et al., 1996, Leibovitch et al., 1995, Hurd et al., 1996, Lin and Nash, 1995, Pavlidis and Tanouye, 1995, Yokokura et al., 1995, de la Pompa, 1994, Tsunoda and Salkoff, 1995, Hevers and Hardie, 1995, Delgado et al., 1994, Chopra and Singh, 1994, Broadie and Bate, 1993, Broadie and Bate, 1993, Engel and Wu, 1992, Stern and Ganetzky, 1992, Hardie, 1991, Hardie et al., 1991, Balakrishnan and Rodrigues, 1991, Hardie, 1991, Mallart et al., 1991, Gautam and Tanouye, 1990, Komatsu et al., 1990, Singh and Wu, 1990, Budnik et al., 1990, Haugland and Wu, 1990, Ferrus et al., 1990, Stern et al., 1990, Lichtinghagen et al., 1990, Gisselmann et al., 1989, Baumann et al., 1987, Kamb et al., 1987, Ganetzky and Wu, 1983, Ganetzky and Wu, 1982, Madhavan et al., 2000, Hodge et al., 2005, Kuebler et al., 2001, Ping et al., 2011) Sh^ks133 (Mir and Krishnan, 1995)
Name Synonym	Shaker¹⁴ (Vahasoyrinki et al., 2006)
Secondary FlyBase IDs

References ( 76 )

Generate a list of	All references relating to this allele ( 76 )

List References by type	Research paper ( 70 ) Review ( 2 ) Abstract ( 4 )
Recent research papers ( 2 )
	Mozer and Sandstrom, 2012, Mol. Cell. Neurosci. 51(3-4): 89--100 Drosophila neuroligin 1 regulates synaptic growth and function in response to activity and phosphoinositide-3-kinase. [FBrf0219839] Ping et al., 2011, PLoS ONE 6(1): e16043 Shal/K(v)4 Channels Are Required for Maintaining Excitability during Repetitive Firing and Normal Locomotion in Drosophila. [FBrf0212839] Show all research papers ...
Recent reviews (0)
	All reviews listed in FlyBase were published before 2011 Show reviews ...

Allele Dmel\Sh14

Allele Dmel\Sh¹⁴