Allele Dmel\Sh^{EKO.Scer\UAS.T:Avic\GFP-GL}

General Information
Symbol	Dmel\Sh^{EKO.Scer\UAS.T:Avic\GFP-GL}	Species	D. melanogaster
Name		FlyBase ID	FBal0127270
Feature type	allele	Associated gene	Dmel\Sh

Allele class
Mutagen	in vitro construct - regulatory fusion, in vitro construct - coding region fusion, in vitro construct - deletion, in vitro construct - site directed mutagenesis
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class
Mutagen	in vitro construct - coding region fusion (White et al., 2001) in vitro construct - deletion (White et al., 2001) in vitro construct - regulatory fusion (White et al., 2001) in vitro construct - site directed mutagenesis (White et al., 2001)
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	Sh^29-4.hs (White et al., 2001)
Nature of the lesion	Statement Reference Construct: Amino acid replacement: D316N. Amino acid replacement: K374Q. Scer\UAS sequences drive expression of a mutated form of the 29-4 Sh that has had amino acid residues 1-29 replaced with the coding sequence of T:Avic\GFP^GL. (White et al., 2001)
Carried in construct	P{UAS-EKO⁺} (Rodriguez Moncalvo and Campos, 2005, Fergestad et al., 2006, Osterwalder et al., 2001, Osterwalder et al., 2001, White et al., 2001, Ishimoto et al., 2005, Luan et al., 2006, Mosca et al., 2005, White et al., 2001, Joiner et al., 2006, Peabody et al., 2008, Peabody et al., 2009, Parisky et al., 2008, Crocker et al., 2010, Rajan and Perrimon, 2012, Duch et al., 2008, Freeman et al., 2010)
Tagged with	T:Avic\GFP^GL (Osterwalder et al., 2001, Osterwalder et al., 2001, White et al., 2001, Ishimoto et al., 2005, Rodriguez Moncalvo and Campos, 2005, Fergestad et al., 2006, Luan et al., 2006, Mosca et al., 2005)
Cytology
Phenotypic Data
Phenotypic Class
	behavior defective \| RU486 conditional, with Scer\GAL4^{Mef2.247.Switch} (Joiner et al., 2006) body color defective \| adult stage A1, with Scer\GAL4^burs.PP (Peabody et al., 2008) body color defective \| adult stage A1, with Scer\GAL4^dimm-929 (Peabody et al., 2008) circadian behavior defective \| adult stage, with Scer\GAL4^P2.4.Pdf (Parisky et al., 2008) flight defective, with Scer\GAL4^futsch-C380, Scer\GAL80^Cha.PK (Duch et al., 2008) lethal, with Scer\GAL4^elav.PLu (Osterwalder et al., 2001) lethal, with Scer\GAL4^elav-C155 (White et al., 2001) lethal, with Scer\GAL4^how-24B (Osterwalder et al., 2001, White et al., 2001) locomotor behavior defective, with Scer\GAL4^how-24B (White et al., 2001) neurophysiology defective, with Scer\GAL4^{Mhc.Switch.PO} (Osterwalder et al., 2001) neurophysiology defective, with Scer\GAL4^NP1535 (Ishimoto et al., 2005) neurophysiology defective \| adult stage, with Scer\GAL4^futsch-C380, Scer\GAL80^Cha.PK (Duch et al., 2008) neurophysiology defective \| RU486 conditional, with Scer\GAL4^{Mhc.Switch.PO} (Osterwalder et al., 2001) sleep defective, with Scer\GAL4^Ilp2.PR (Crocker et al., 2010) taste perception defective, with Scer\GAL4^NP1535 (Ishimoto et al., 2005) visible \| cold sensitive, with Scer\GAL4^burs.PP (Peabody et al., 2008) visible \| cold sensitive, with Scer\GAL4^Ccap.PP (Peabody et al., 2008) visual behavior defective \| larval stage, with Scer\GAL4^GMR.PF (Rodriguez Moncalvo and Campos, 2005)
Phenotype Manifest In
	abdomen \| adult stage A1, with Scer\GAL4^burs.PP (Peabody et al., 2008) abdomen \| adult stage A1, with Scer\GAL4^dimm-929 (Peabody et al., 2008) adult cuticle, with Scer\GAL4^A307 (White et al., 2001) adult cuticle, with Scer\GAL4^Ccap.PP (Luan et al., 2006) embryonic/larval neuron, with Scer\GAL4^elav-C155 (White et al., 2001) eye, with Scer\GAL4^GMR.PF (White et al., 2001) larval head, with Scer\GAL4^Ccap.PP (Luan et al., 2006) leg, with Scer\GAL4^Ccap.PP (Luan et al., 2006) motor neuron, with Scer\GAL4^elav-C155 (White et al., 2001) photoreceptor, with Scer\GAL4^GMR.PF (White et al., 2001) presumptive embryonic/larval muscle system, with Scer\GAL4^elav-C155 (White et al., 2001) presumptive embryonic/larval muscle system, with Scer\GAL4^how-24B (White et al., 2001) synapse, with Scer\GAL4^elav-C155 (White et al., 2001) wing, with Scer\GAL4^A307 (White et al., 2001) wing, with Scer\GAL4^Ccap.PP (Luan et al., 2006, Peabody et al., 2009) wing \| adult stage A1 \| cold sensitive, with Scer\GAL4^burs.PP (Peabody et al., 2008) wing \| adult stage A1 \| cold sensitive, with Scer\GAL4^Ccap.PP (Peabody et al., 2008)
Detailed Description
	Statement Reference Expression of Sh[EKO.Scer\UAS.T:Avic\GFP-GL] in Scer\GAL4[Ilp2.PR]-neurons results in an increase in sleep both during the day and night. (Crocker et al., 2010) Expression of one, two, or three copies of Sh[EKO.Scer\UAS.T:Avic\GFP-GL] in N[[CCAP]] neurons under the control of Scer\GAL4[Ccap.PP] induces wing expansion deficits of increasing severity and frequency. Suppression of N[[CCAP]] by three copies of Sh[EKO.Scer\UAS.T:Avic\GFP-GL] completely eliminates both the tonic abdominal contraction that defines the grooming phase and air swallowing. Despite the absence of the expansion phase, however, the duration of the perch selection phase in these animals is indistinguishable from that of control flies. Flies expressing two copies of Sh[EKO.Scer\UAS.T:Avic\GFP-GL] in N[[CCAP]] neurons under the control of Scer\GAL4[Ccap.PP] can be divided into two categories: Approximately half resemble flies expressing one copy of Sh[EKO.Scer\UAS.T:Avic\GFP-GL], which exhibit a robust expansion phase that includes tonic abdominal contraction and air swallowing, while the rest resemble flies expressing three copies of Sh[EKO.Scer\UAS.T:Avic\GFP-GL], which completely lack an expansion phase. (Peabody et al., 2009) Expression of two copies of Sh[EKO.Scer\UAS.T:Avic\GFP-GL] under the control of Scer\GAL4[futsch-C380] in the presence of Scer\GAL80[Cha.PK] (to suppress expression in all cholinergic neurons) results in the MN5 neuron showing strongly decreased excitability in response to a current injection into the soma. Resting membrane potential and input resistance of the MN5 neuron are unaffected. The dendritic structure of the MN5 neuron is altered compared to wild type in animals expressing two copies of Sh[EKO.Scer\UAS.T:Avic\GFP-GL] under the control of Scer\GAL4[futsch-C380]. Total dendritic length and the the mean length of individual dendritic branches is increased. The number of branch points and maximum branch order are unaffected. The mean distance of all dendritic segments to the origin of the tree and the total dendritic surface are increased. Flies expressing two copies of Sh[EKO.Scer\UAS.T:Avic\GFP-GL] under the control of Scer\GAL4[futsch-C380] in the presence of Scer\GAL80[Cha.PK] show reduced flight motor performance in a restrained flight assay. The initial and total flight time are significantly decreased compared to wild type. (Duch et al., 2008) Expression of Sh[EKO.Scer\UAS.T:Avic\GFP-GL] by Scer\GAL4[P2.4.Pdf] results in an increase of sleep but a decrease in sleep latency in the day and night, compared to controls. (Parisky et al., 2008) Most animal expressing one copy of Sh[EKO.Scer\UAS.T:Avic\GFP-GL] by Scer\GAL4[burs.PP] show a partially expanded wing phenotype, a small fraction do not expand their wings, and 40% show normal wing expansion. In contrast, most flies expressing three copies of Sh[EKO.Scer\UAS.T:Avic\GFP-GL] fail to expand their wings. These animals also fail to tan properly, retaining their unpigmented juvenile state 3 hours after eclosion. Flies expressing a single copy of Sh[EKO.Scer\UAS.T:Avic\GFP-GL] under the control of Scer\GAL4[Ccap.PP] fail to expand their wings when raised at 18[o]C, but expand their wings normally when raised at 31[o]C. Similarly, flies expressing a single copy of Sh[EKO.Scer\UAS.T:Avic\GFP-GL] by Scer\GAL4[burs.PP] show approximately five-fold higher frequency in wing expansion defects when raised at 18[o]C than when raised at 31[o]C. A fraction of these animals raised at 18[o]C then shifted to 31[o]C from 5 to 6 days after puparium formation show wing expansion defects. Although adult flies expressing three copies of Sh[EKO.Scer\UAS.T:Avic\GFP-GL] under the control of Scer\GAL4[dimm-929] fail to expand their wings, they consistently show a period of sustained abdominal contraction characteristic of the wing expansion phase after eclosion and they ingest air similarly to wild-type flies. However, in contrast to wild-type flies, the abdomen is elongated and constricted, but not necessarily flexed. Only 4% of adults expressing three copies of Sh[EKO.Scer\UAS.T:Avic\GFP-GL] under the control of Scer\GAL4[burs.PP] show sustained abnormal abdominal contractions during the wing expansional phase after eclosion, and only 14% swallow air (all mutant animals that swallow air are female). (Peabody et al., 2008) Expression of Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} under the control of Scer\GAL4^{Mef2.247.Switch} (in the presence of RU486) causes a significant increase in sleep. (Joiner et al., 2006) Expression of increasing copy numbers of Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} in the wing under the control of Scer\GAL4^Ccap.PP results in incremental increases in the frequency and severity of wing expansion deficits. Most flies expressing 1xSh^{EKO.Scer\UAS.T:Avic\GFP-GL} partially expand their wings, whereas all flies expressing 3xSh^{EKO.Scer\UAS.T:Avic\GFP-GL} have unexpanded wings. Flies expressing 2xSh^{EKO.Scer\UAS.T:Avic\GFP-GL} (under the control of Scer\GAL4^Ccap.PP), typically lack the level of pigmentation observed in age-matched controls 3hrs after eclosion. Inhibition of melanisation in these flies appears complete, with the differences in cuticle pigmentation between Sh^{EKO.Scer\UAS.T:Avic\GFP-GL}-expressing and control flies comparable with those between newly eclosed and 3hr-old wild-type flies. A small number of animals expressing 3xSh^{EKO.Scer\UAS.T:Avic\GFP-GL} (under the control of Scer\GAL4^Ccap.PP) die with head eversion defects and foreshortened wings and legs. Pharate adults expressing 3xSh^{EKO.Scer\UAS.T:Avic\GFP-GL} (under the control of Scer\GAL4^Ccap.PP) exhibit no loss of N_CCAP neurons. Expression of Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} (under the control of Scer\GAL4^dimm-929) incrementally increases the severity of wing expansion deficits with increasing transgene copy numbers, with expression of 3xSh^{EKO.Scer\UAS.T:Avic\GFP-GL} resulting in unexpanded wings in 100% of animals and failure to tan. Flies expressing Scer\GAL80^Ccap, as well as Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} (under the control of Scer\GAL4^dimm-929) exhibited wild-type levels of wing expansion. (Luan et al., 2006) Flies expressing Sh^{EKO.Scer\UAS.T:Avic\GFP-GL}, under the control of Scer\GAL4^NP1535, exhibit a significantly lowered proboscis extension reflex rate in response to 100mM sucrose. The gustatory receptor neuron response to 100mM sucrose is reduced in these flies. (Ishimoto et al., 2005) Expression of Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} in Rh6 photoreceptors, under the control of Scer\GAL4^Rh6.PD, does not affect 5-HT arborization. Expression of Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} in all photoreceptors, under the control of Scer\GAL4^GMR.PF, does not affect 5-HT arborization, but does reduce larval response to light. (Rodriguez Moncalvo and Campos, 2005) When Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} is driven by Scer\GAL4^elav.PLu, it is embryonic lethal. When Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} is driven by Scer\GAL4^how-24B, larvae survive until third instar. When Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} under the control of Scer\GAL4^{Mhc.Switch.PO} in the presence of RU486, K⁺ currents on MF6 (in abdominal segments 2-4) are abnormal. Outward K⁺ currents of about 315nA are seen at a holding potential of +20mV a seven fold increase over controls. When RU486 is not present 36% increase in current is seen over controls. (Osterwalder et al., 2001) When Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} is driven by Scer\GAL4^how-24B the number and gross morphology of the sensory neurons appears unaltered. When Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} is driven by Scer\GAL4^elav-C155 or Scer\GAL4^how-24B K⁺ current densities in embryonic neurons and muscles respectively are over 2-fold larger than those of controls. Tha activation threshold of these currents is also substantially shifted in the hyperpolarising direction in both cell types: -30 mV in neurons and -26 in muscles. Expression of Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} significantly reduces cellular excitability and indeed no muscle contractions are seen in mutant muscle fibres. Decreases in both input resistances and resting membrane potentials are seen in muscles. On average, resting potentials are hyperpolarised by -9mV in mutant muscles and input resistances measured at the resting potential are 74% smaller. When synaptic function in muscle fibre is measured in response to retrograde stimulation of axon 2 in the segmental nerve, while excitatory postsynaptic currents (EPSCs) are similar to controls excitatory postsynaptic potentials (EPSPs) are on average 30% smaller and decay nearly five times as fast. Expression of one copy of Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} driven by either Scer\GAL4^elav-C155 or Scer\GAL4^how-24B leads to increased mortality. Two copies are lethal. If two copies of are driven by Scer\GAL4^elav-C155, 99% of embryos fail to hatch. When driven by Scer\GAL4^how-24B lethality is primarily in larval and pupal stages. This lethality is dosage dependant. In both nerves and muscles, the increasing lethality with increasing dosage correlates with progressive impairment to motor functions. Mutant embryos with the Scer\GAL4^elav-C155 driver show a reduction in the frequency of full-body peristaltic waves. When the VLM innervation pattern of mutant embryos with the Scer\GAL4^elav-C155 driver are examined at late stage 17, just after developmental arrest, abnormalities are seen. There is an approximately 100% increase in both the frequency and average length of the collateral branches. No defects are seen in these ectopic synapses. When Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} is driven by Scer\GAL4^GMR.PF, defects are seen in the eye's response to a light stimulus. the initial amplitude of the photoreceptor potential declines progressively with increasing transgene copy number, with suppression saturating at approximately 50% of controls. In contrast, the postsynaptic response of the laminar interneurons remains relatively invariant. When three copies of the transgene responsible for Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} are driven by Scer\GAL4^A307 various anatomical and behavioural defects are seen. There is pronounced pigmentation of the thoracic trident, a failure of wing expansion. Neither of these defects are seen with two copies of P{UAS-EKO⁺}. (White et al., 2001)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT Enhancer of
Statement Reference Scer\GAL4^hs.2sev/Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} is a non-enhancer of short lived \| dominant phenotype of Atpα^DTS1 (Fergestad et al., 2006) Sh^{EKO.Scer\UAS.T:Avic\GFP-GL}/Scer\GAL4^elav.PLu is a non-enhancer of short lived \| dominant phenotype of Atpα^DTS1 (Fergestad et al., 2006)
Suppressor of
Statement Reference Scer\GAL4^futsch-C380/Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} is a suppressor of neuroanatomy defective \| larval stage phenotype of Ca-P60A^Kum170, comt⁶ (Freeman et al., 2010) Scer\GAL4^futsch-C380/Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} is a suppressor of neurophysiology defective \| larval stage phenotype of Ca-P60A^Kum170, comt⁶ (Freeman et al., 2010)
NOT Suppressor of
Statement Reference Scer\GAL4^Ilp3.PB/Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} is a non-suppressor of small body \| adult stage phenotype of upd2^Δ3-62 (Rajan and Perrimon, 2012)
Phenotype Manifest In
Enhanced by
Statement Reference Scer\GAL4^A307, Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} has wing phenotype, enhanceable by para^ts1 (White et al., 2001)
Suppressor of
Statement Reference Scer\GAL4^futsch-C380/Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} is a suppressor of neuromuscular junction \| larval stage phenotype of Ca-P60A^Kum170, comt⁶ (Freeman et al., 2010)
NOT Suppressor of
Statement Reference Scer\GAL4^Ilp3.PB/Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} is a non-suppressor of wing phenotype of upd2^Δ3-62 (Rajan and Perrimon, 2012)
Additional Comments
Genetic Interactions
Statement Reference Expression of Sh[EKO.Scer\UAS.T:Avic\GFP-GL] under the control of Scer\GAL4[futsch-C380] suppresses the increased synaptic growth and transmitter release observed at the neuromuscular junction in comt[6] Ca-P60A[Kum170] larvae. (Freeman et al., 2010) There is no significant change in the lifespan of Atpα^DTS1 mutants when they express Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} under the control of either Scer\GAL4^elav.PLu or Scer\GAL4^hs.2sev. (Fergestad et al., 2006) 79% of para^ts1 flies expressing two copies of P{UAS-EKO⁺} (driven by Scer\GAL4^A307) fail to expand their wings. (White et al., 2001)
Xenogenetic Interactions
Statement Reference Expression of Sh[EKO.Scer\UAS.T:Avic\GFP-GL] under the control of Scer\GAL4[Ilp3.PB] does exacerbate the reduced wing area phenotype of upd2[Δ3-62] mutants. (Rajan and Perrimon, 2012)
Complementation & Rescue Data
Comments
Stocks ( 3 )
Bloomington	40973 y¹ w^; wg^Sp-1/CyO; P{UAS-EKO⁺}323 40974 y¹ w^; P{UAS-EKO⁺}222a P{UAS-EKO⁺}222b 40975 y¹ w^*; P{UAS-EKO⁺}222a P{UAS-EKO⁺}222b; P{UAS-EKO⁺}323
Notes on Origin
Discoverer

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 1 )
Reported As
Symbol Synonym	Sh^{EKO.Scer\UAS.T:Avic\GFP-GL}
Name Synonym
Secondary FlyBase IDs

References ( 17 )
Research paper	Rajan and Perrimon, 2012, Cell 151(1): 123--137 Drosophila cytokine unpaired 2 regulates physiological homeostasis by remotely controlling insulin secretion. [FBrf0219535] Crocker et al., 2010, Neuron 65(5): 670--681 Identification of a Neural Circuit that Underlies the Effects of Octopamine on Sleep:Wake Behavior. [FBrf0210214] Freeman et al., 2010, Brain Res. 1326: 15--29 A new genetic model of activity-induced Ras signaling dependent pre-synaptic plasticity in Drosophila. [FBrf0210453] Peabody et al., 2009, J. Neurosci. 29(11): 3343--3353 Characterization of the decision network for wing expansion in Drosophila using targeted expression of the TRPM8 channel. [FBrf0207505] Duch et al., 2008, J. Neurophysiol. 100(5): 2525--2536 Dendrite elongation and dendritic branching are affected separately by different forms of intrinsic motoneuron excitability. [FBrf0207189] Parisky et al., 2008, Neuron 60(4): 672--682 PDF cells are a GABA-responsive wake-promoting component of the Drosophila sleep circuit. [FBrf0206340] Peabody et al., 2008, J. Neurosci. 28(53): 14379--14391 Bursicon functions within the Drosophila CNS to modulate wing expansion behavior, hormone secretion, and cell death. [FBrf0206568] Fergestad et al., 2006, Genetics 172(2): 1031--1042 Neuropathology in Drosophila membrane excitability mutants. [FBrf0190718] Joiner et al., 2006, Nature 441(7094): 757--760 Sleep in Drosophila is regulated by adult mushroom bodies. [FBrf0192316] Luan et al., 2006, J. Neurosci. 26(2): 573--584 Functional dissection of a neuronal network required for cuticle tanning and wing expansion in Drosophila. [FBrf0191050] Ishimoto et al., 2005, EMBO J. 24(18): 3259--3265 G-protein gamma subunit 1 is required for sugar reception in Drosophila. [FBrf0187509] Mosca et al., 2005, Proc. Natl. Acad. Sci. U.S.A. 102(9): 3477--3482 Dissection of synaptic excitability phenotypes by using a dominant-negative Shaker K+ channel subunit. [FBrf0191470] Rodriguez Moncalvo and Campos, 2005, Dev. Biol. 286(2): 549--558 Genetic dissection of trophic interactions in the larval optic neuropil of Drosophila melanogaster. [FBrf0190156] Osterwalder et al., 2001, Proc. Natl. Acad. Sci. U.S.A. 98(22): 12596--12601 A conditional tissue-specific transgene expression system using inducible GAL4. [FBrf0139796] White et al., 2001, Neuron 31(5): 699--711 Targeted attenuation of electrical activity in Drosophila using a genetically modified K[+] channel. [FBrf0139774]
Abstract	Osterwalder et al., 2001, Bellen, Taylor, 2001: 83 A GAL4/UAS based system for conditional, tissue-specific transgene expression. [FBrf0144631] White et al., 2001, Bellen, Taylor, 2001: 62 Homeostatic changes in synaptic function following electrical inhibition of the photoreceptor response. [FBrf0144707]

Allele Dmel\ShEKO.Scer\UAS.T:Avic\GFP-GL

Allele Dmel\Sh^{EKO.Scer\UAS.T:Avic\GFP-GL}