Allele Dmel\EcR^{A-ΔC655.F645A.Scer\UAS}

General Information
Symbol	Dmel\EcR^{A-ΔC655.F645A.Scer\UAS}	Species	D. melanogaster
Name		FlyBase ID	FBal0190469
Feature type	allele	Associated gene	Dmel\EcR

Allele class
Mutagen	in vitro construct - regulatory fusion, in vitro construct - amino acid replacement
Recent Updates
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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
Mutagen	in vitro construct - amino acid replacement (Brown et al., 2006) in vitro construct - regulatory fusion (Brown et al., 2006)
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 Construct: Amino acid replacement: F645A. Scer\UAS regulatory sequences drive expression of a mutated EcR A isoform, with the above amino acid replacement, that is truncated after residue 655. (Brown et al., 2006)
Carried in construct	P{UAS-EcR.A.F645A} (Brown et al., 2006, Cakouros et al., 2008, Mitchell et al., 2008, Liu et al., 2010, Sinenko et al., 2010)
Cytology
Phenotypic Data
Phenotypic Class
	lethal \| pharate adult stage, with Scer\GAL4^repo (Liu et al., 2010) mitotic cell cycle defective \| somatic clone, with Scer\GAL4^Act5C.PP (Mitchell et al., 2008) neuroanatomy defective, with Scer\GAL4^Fmrf.PS (Brown et al., 2006) neuroanatomy defective, with Scer\GAL4^Mhc.PW (Liu et al., 2010)
Phenotype Manifest In
	eye (Cakouros et al., 2008) neurohemal organ, with Scer\GAL4^Fmrf.PS (Brown et al., 2006) ommatidium, with Scer\GAL4^GMR.PF (Cakouros et al., 2008) pigment cell, with Scer\GAL4^GMR.PF (Cakouros et al., 2008) synapse, with Scer\GAL4^Mhc.PW (Liu et al., 2010) Tv neuron & axon, with Scer\GAL4^Fmrf.PS (Brown et al., 2006) wing disc \| somatic clone, with Scer\GAL4^Act5C.PP (Mitchell et al., 2008)
Detailed Description
	Statement Reference Muscle expression of EcR[A-ΔC655.F645A.Scer\UAS] under the control of Scer\GAL4[Mhc.PW] produces a delay in synapse elimination due to post-synaptic disruption of EcR signaling. Expression of EcR[A-ΔC655.F645A.Scer\UAS] in presynaptic neurons (under the control of Scer\GAL4[OK6] does not delay synapse elimination. Expression of EcR[A-ΔC655.F645A.Scer\UAS] postsynaptically (under the control of Scer\GAL4[OK6]) in 9 hour APF pupae does not induce presynaptic dismantling such as synaptic vesicle aggregation, decreased bouton number, or enlarged bouton size, while post-synaptic dismantling occurs normally. (Liu et al., 2010) Specific overexpression of EcR[A-ΔC655.F645A.Scer\UAS] in the eye, under the control of Scer\GAL4[GMR.PF], disrupts differentiation of the ommatidia and eye patterning. This results in a decrease in pigment cells, collapse of the eye, and characteristic scarring. Inhibition of EcR function by the expression of EcR[A-ΔC655.F645A.Scer\UAS] under the control of Scer\GAL4[e22c] has no effect on wing size. (Cakouros et al., 2008) BrdU incorporation and the number of mitotic cells is reduced in clones in the wing disc expressing EcR[A-ΔC655.F645A.Scer\UAS] under the control of Scer\GAL4[Act5C.PP] compared to control clones. (Mitchell et al., 2008) Thoracic ventral neurosecretory cells that express EcR^{A-ΔC655.F645A.Scer\UAS} under the control of Scer\GAL4^Fmrf.PS are of normal size and larval morphology at the start of metamorphosis. However, these mutants show defective neuronal remodelling during metamorphosis. The axons show much lower levels of pruning compared to wild-type cells and show no filopodia during the pruning phase. (Brown et al., 2006)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement Reference EcR^{A-ΔC655.F645A.Scer\UAS}, Scer\GAL4^Hml.Δ is an enhancer of increased cell number \| third instar larval stage phenotype of Hsap\RUNX1::Hsap\RUNX1T1^Scer\UAS.cSa, Scer\GAL4^Hml.Δ (Sinenko et al., 2010)
Phenotype Manifest In
Suppressed by
Statement Reference EcR^{A-ΔC655.F645A.Scer\UAS}, Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF has ommatidium phenotype, suppressible by EcR^{A-ΔC655.F645A.Scer\UAS}, Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF (Cakouros et al., 2008, Cakouros et al., 2008) EcR^{A-ΔC655.F645A.Scer\UAS}, Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF has pigment cell phenotype, suppressible by EcR^{A-ΔC655.F645A.Scer\UAS}, Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF (Cakouros et al., 2008, Cakouros et al., 2008) EcR^{A-ΔC655.F645A.Scer\UAS} has eye phenotype, suppressible by Scer\GAL4^GMR.PF/EcR^{A-ΔC655.F645A.Scer\UAS}/Scer\GAL4^GMR.PF (Cakouros et al., 2008, Cakouros et al., 2008)
Enhancer of
Statement Reference EcR^{A-ΔC655.F645A.Scer\UAS}, Scer\GAL4^Hml.Δ is an enhancer of embryonic/larval hemocyte \| third instar larval stage phenotype of Hsap\RUNX1::Hsap\RUNX1T1^Scer\UAS.cSa, Scer\GAL4^Hml.Δ (Sinenko et al., 2010)
Suppressor of
Statement Reference EcR^{A-ΔC655.F645A.Scer\UAS}, Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF is a suppressor of ommatidium phenotype of EcR^{A-ΔC655.F645A.Scer\UAS}, Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF (Cakouros et al., 2008, Cakouros et al., 2008) EcR^{A-ΔC655.F645A.Scer\UAS}, Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF is a suppressor of pigment cell phenotype of EcR^{A-ΔC655.F645A.Scer\UAS}, Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF (Cakouros et al., 2008, Cakouros et al., 2008) Scer\GAL4^e22c/EcR^{A-ΔC655.F645A.Scer\UAS} is a suppressor of wing phenotype of LKR^{dsRNA.Scer\UAS} (Cakouros et al., 2008) Scer\GAL4^GMR.PF, EcR^{A-ΔC655.F645A.Scer\UAS}, Scer\GAL4^GMR.PF is a suppressor of eye phenotype of EcR^{A-ΔC655.F645A.Scer\UAS} (Cakouros et al., 2008, Cakouros et al., 2008)
Additional Comments
Genetic Interactions
Statement Reference Knock-down of LKR through LKR[IR.Scer\UAS] partially restores the pigmentation defect found in EcR[A-ΔC655.F645A.Scer\UAS] (Scer\GAL4[GMR.PF]) mutants and display a striking decrease of scarring compared to expression of EcR[A-ΔC655.F645A.Scer\UAS] (Scer\GAL4[GMR.PF]) alone. Expression of EcR[A-ΔC655.F645A.Scer\UAS] restores the small wing phenotype caused by LKR[IR.Scer\UAS]. (Cakouros et al., 2008)
Xenogenetic Interactions
Statement Reference Expression of EcR[A-ΔC655.F645A.Scer\UAS] slightly enhances the hemocyte overproliferation seen in third instar larvae when Hsap\RUNX1::Hsap\RUNX1T1[Scer\UAS.cSa] is expressed under the control of Scer\GAL4[Hml.Δ]. (Sinenko et al., 2010)
Complementation & Rescue Data
Comments
Stocks ( 1 )
Bloomington	9452 w^*; P{UAS-EcR.A.F645A}TP2
Notes on Origin
Discoverer

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 1 )
Reported As
Symbol Synonym	EcR^{A-ΔC655.F645A.Scer\UAS}
Name Synonym
Secondary FlyBase IDs

References ( 5 )
Research paper	Liu et al., 2010, J. Neurosci. 30(35): 11624--11634 Distinct Presynaptic and Postsynaptic Dismantling Processes of Drosophila Neuromuscular Junctions during Metamorphosis. [FBrf0211694] Sinenko et al., 2010, Blood 116(22): 4612--4620 Genetic manipulation of AML1-ETO-induced expansion of hematopoietic precursors in a Drosophila model. [FBrf0212361] Cakouros et al., 2008, J. Cell Biol. 182(3): 481--495 dLKR/SDH regulates hormone-mediated histone arginine methylation and transcription of cell death genes. [FBrf0205793] Mitchell et al., 2008, Development 135(16): 2707--2716 The Ecdysone-inducible zinc-finger transcription factor Crol regulates Wg transcription and cell cycle progression in Drosophila. [FBrf0207008] Brown et al., 2006, Development 133(2): 275--285 Use of time-lapse imaging and dominant negative receptors to dissect the steroid receptor control of neuronal remodeling in Drosophila. [FBrf0190279]

Allele Dmel\EcRA-ΔC655.F645A.Scer\UAS

Allele Dmel\EcR^{A-ΔC655.F645A.Scer\UAS}