Open Close
General Information
Symbol
Dmel\EcRB1-ΔC655.F645A.UAS
Species
D. melanogaster
Name
FlyBase ID
FBal0141829
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-EcRDN, UAS-EcR-F645A, UAS-EcRF645A, EcR-DN, EcRF645A, UAS-EcR.B1-ΔC655.F645A, UAS-EcR-DN, EcR-F645A, P{UAS-EcR.B1-DeltaC655.F645A}, EcR-B1-F645A
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Carried in construct
Cytology
Nature of the lesion
Statement
Reference

UASt regulatory sequences drive expression of a mutated EcR B1 isoform which ends at EcR amino acid residue 655 and has the amino acid replacement F465A.

Allele components
Product class / Tool use(s)
Encoded product / tool
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 ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

glial cell & brain & pupa | conditional ts, with Scer\GAL4Tab2-201Y

mesothoracic ventral neurosecretory neuron & axon, with Scer\GAL4FMRFa.PS

metathoracic ventral thoracic neurosecretory neuron & axon, with Scer\GAL4FMRFa.PS

neuron & ventral nerve cord, with Scer\GAL4Crz.PC

prothoracic ventral neurosecretory neuron & axon, with Scer\GAL4FMRFa.PS

Detailed Description
Statement
Reference

The expression of EcRB1-ΔC655.F645A.UAS under the control of Scer\GAL4byn-Gal4 throughout metamorphosis results in adults that die soon after eclosion, show an enlarged pylorus and lacking ileum histolysis.

Expressing EcRB1-ΔC655.F645A.UAS under the control of Scer\GAL4CCAP.PP results in the loss of most CCAP neurons in wandering third instar larvae and severely defective pupal development, characterized by a failure in head eversion and shortened wings and legs.

Expression of EcRB1-ΔC655.F645A.UAS under the control of Scer\GAL4NP3056, Scer\GAL4orb-0449-G4 or Scer\GAL4lilli-189Y in combination with a Gal80[ts] transgene to restrict expression to between late third instar larva and 24 hours after puparium formation, results in the retention of larval innervation patterns of these antennal lobe local interneurons that are lost from controls during metamorphosis.

Expression of EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4phm.PO leads to accumulation of lipid droplets in the prothoracic gland cells of third instar larvae.

Expression of EcRB1-ΔC655.F645A.Scer\UAS in salivary glands during embryonic and early larval stages does not affect normal development.

Expression of EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4c42 results in delayed development and larval lethality at the early first instar stage. Larvae are smaller in size, slow moving, and display gross abnormalities including low adipose tissue, transparent cuticle and deformed Malpighian tubules.

Malpighian tubule defects of first instar larvae expressing EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4c42 include reduction in overall size, failure to properly elongate and remaining coiled, smaller mean diameter, reduction of the number of and irregular distribution of stellate cells and principal cells in anterior and posterior Malpighian tubules, and reduction in uric acid deposition as compared to wild type.

Animals expressing EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4Sgs3.PD show normal mid-third instar (wandering behaviour) and late larval (everting anterior spiracles, barrel shape, midgut programmed cell death) ecdysone-triggered responses. The prepupal ecdysone-triggered responses (head eversion, wing and leg inflation and leg extension) also occur normally. In the salivary gland, mid-third instar glue synthesis, late larval glue secretion and prepupal salivary gland programmed cell death are all defective.

Expression of EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4Sgs3.PD blocks the formation of the large acidic structures which normally occurs in salivary gland cells approximately 1.5 hours after head eversion, and also blocks caspase activation at 2 hours after head eversion. This results in a persistent salivary gland phenotype at 24 hours after puparium formation.

Expression of EcRB1-ΔC655.F645A.Scer\UAS in astrocytes, under the control of Scer\GAL4alrm.PD, does not affect astrocyte morphology in 3rd instar larvae. However, EcRB1-ΔC655.F645A.Scer\UAS expression completely blocks their morphological transformation into the highly vacuolated morphology apparent in controls at 6 hours after pupal formation.

Astrocyte morphological transformation can be suppressed when EcRB1-ΔC655.F645A.Scer\UAS is expressed in one to two astrocytes, using MARCM, rather than the entire population. EcRB1-ΔC655.F645A.Scer\UAS expression block the induction of phagolysomal activity.

Expression of EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4RapGAP1-OK6 results in the transverse nerve making ectopic connections at the larval neuromuscular junction.

Expression of EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4RapGAP1-OK6 results in the formation of ectopic connections at the larval neuromuscular junction.

Over 95% of larvae expressing EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4ETH.Switch in the presence of RU486 have multiple mouthparts (indicating a failure to complete ecdysis), and approximately 70% of these animals die as larvae.

Severing of the dendrites of ddaC neurons occurs in animals expressing EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4repo does occur, albeit with some delay. However, the glial membranes that wrap the proximal dendrites as part of this dendrite pruning process show very little sign of retraction or disintegration by 16 hours after puparium formation and the wrapped dendrite segments remain intact. This defect persist until the death of the neurons during metamorphosis.

Induction of EcRB1-ΔC655.F645A.Scer\UAS during 0-30 hours after pupal formation (under the control of Scer\GAL80ts.αTub84B and Scer\GAL4wg-IS650) blocks apoptosis and results in rearrangement of the wing margin cells. In addition, blocking ecdysone signalling results in overlap of the double-row hairs in the adult wing.

Larvae expressing EcRB1-ΔC655.F645A.Scer\UAS under the control of either Scer\GAL4tsh-c724 or Scer\GAL4c649 are smaller in size than age-matched controls, with the reduction in size being greatest with the Scer\GAL4tsh-c724 driver.

Larvae expressing EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4c649 contain both first and second instar larval mouth hooks (showing a defect in moulting) at a time when control larvae have already reached the third larval instar stage.

The mean diameter of the Malpighian tubules of larvae expressing EcRB1-ΔC655.F645A.Scer\UAS under the control of either Scer\GAL4tsh-c724 or Scer\GAL4c649 is smaller than that of controls, with the decrease being greatest with the Scer\GAL4tsh-c724 driver. The number of principal cells in the anterior and posterior Malpighian tubules of the mutant larvae is similar to that in wild type. However, the number of stellate cells in the mutant anterior and posterior Malpighian tubules is reduced compared to wild type, with the reduction being greatest with the Scer\GAL4tsh-c724 driver. In addition, the distribution of the stellate cells is altered in the mutant tubules, so that they are present in clusters instead of being evenly distributed as occurs in wild type.

High expression of EcRB1-ΔC655.F645A.Scer\UAS in muscle under the control of Scer\GAL4C57 results in first-instar larval lethality. Lower expression under the control of Scer\GAL4Mhc.PW leads to pupal lethality. Expression under the control of Scer\GAL4Mhc.PW produces a delay in synapse elimination due to post-synaptic disruption of EcR signaling.

Expression of EcRB1-ΔC655.F645A.Scer\UAS postsynaptically (under the control of Scer\GAL4Mhc.PW) results in the complete blockage of both pre- and post-synaptic synapse elimination in pupae 9 hours after puparium formation.

Flies expressing EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4Lsp2.PH have a normal total lipid content.

Expression of EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4slbo.2.6 results in incomplete border cell migration in 60% of stage 10 egg chambers at 29[o]C.

Expression of EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4da.Switch.PT in the presence of 1μg ml[-1] RU486 in male flies results in a 24% increase in the median lifespan compared to controls. Higher levels of EcRB1-ΔC655.F645A.Scer\UAS expression (using increasing concentrations of RU486) abolish this positive effect.

Expression of EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4da.Switch.PT in the presence of RU486 in female flies decreases lifespan in a RU486 dose-dependent manner.

Expression of EcRB1-ΔC655.F645A.Scer\UAS in larval epidermal cells, under the control of Scer\GAL4NP0056, blocks the ability of these cells to constrict, extrude and undergo apoptosis. As a result, abdominal morphogenesis does not succeed and larval epidermal cells remain in the abdomen of pharate adult flies, forming part of the epidermis.

Thoracic ventral neurosecretory cells that express EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4Fmrf.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. EcRB1-ΔC655.F645A.Scer\UAS-expressing neurons start extending filopodia after 24 hours APF from the neurohemal organ and in the growth zone below. As this happens, the remnant neurohemal organ partially fragments, resulting in an adult-like arbor with clumped varicosities and a dense centre. Effects on adult axon outgrowth are relatively mild, with axonal arbors slighlty reduced compared to controls.

Expression of EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4Crz blocks programmed cell death in Crz-expressing ventral nerve cord neurons up to 12 hours after pupal formation.

23% of embryos derived from females carrying EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4slbo.2.6 have abnormal dorsal appendages.

When EcRB1-ΔC655.F645A.Scer\UAS is driven by Scer\GAL4arm.PS 100% lethality is seen. at 18oC this occurs during first instar larval stage, at 25oC this can be embryonic.

Inhibition of ecdysone signalling by expression of EcRB1-ΔC655.F645A.Scer\UAS under the regulation of Scer\GAL4ppk.PG results in C4da neurons losing their ability to initiate larval dendrite pruning at 20 hours after pupal formation, with approximately 90% of large dendritic branches being retained after head eversion.

Inhibition of EcR, through expression of EcRB1-ΔC655.F645A.Scer\UAS at the onset of metamorphosis through the regulatory control of Scer\GAL4how-24B and Scer\GAL80ts.αTub84B results in myofibrils that are transversal, indicating that EcRB1-ΔC655.F645A.Scer\UAS prevents terminal chamber differentiation, with nerve terminals not making synaptic contact with the myocytes.

Expression of EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4Tab2-201Y results in lethality at late pupal stages. Mushroom body axons are not pruned during pupal development in these animals (in contrast to wild type). Infiltration of glial processes into the mushroom body lobes is severely suppressed during early pupal development compared to wild-type pupae.

When expression is governed by Scer\GAL4Lsp2.PH in the larval fat body early autophagosomal structures are able to form but do not acidify, perhaps due to a failure to fuse with lysosomes.

Expression of EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4Act5C.PI results in lethality either during embryonic development or soon after hatching. Expression of EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4GMR.PF usually results in animals ceasing development after pupariation. Escapers have defective eyes, with poorly pigmented ommatidia and large necrotic, melanised patches. At 25oC, most animals expressing EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4dpp.blk1 fail to pupate. At 20oC, some animals arrest before pupation, while most pupate but die during adult development. Escapers are morphologically normal except for the orientation and sometimes length of the posterior scutellar bristles. Animals expressing EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4Ser.PGF fail to pupate. Pupariation is defective in animals expressing EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4Eip71CD.657; the animals fail to shorten and tanning occurs only at the extremities (where the Scer\GAL4Eip71CD.657 driver is not expressed). The imaginal discs do not evert. The salivary glands histolyse on schedule at pupation in animals expressing EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4Sgs3.PD. The polytene chromosomes are normal in size, but their puffing pattern in white prepupae remains blocked at puff stage 1' (PS1'), a stage normally seen only early in the third larval instar. The fat body cells fail to dissociate at pupation in animals expressing EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4Lsp2.PH. Most of the animals die late in adult development. Viability is lower in females than in males. Most animals expressing EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4Eh.0.8 moult into adult but fail to expand their wings. Border cell migration is delayed or fails completely in females expressing EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4slbo.2.6. The chorion structures are fragile and eggs derived from these females collapse soon after oviposition. Dorsal appendages are frequently broad or branched and operculum structures are poorly developed.

Expression of EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4hs.PB using heat shock for 3 to 5 hours after egg laying results in embryonic lethality, with highly penetrant defects in germ band retraction, head involution and cuticle deposition. Expression of EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4LP1, Scer\GAL469B or Scer\GAL4c381 results in embryonic and first larval instar lethality with a low penetrance of germ band retraction defects. Expression of EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL469B or Scer\GAL4c381 in an EcRM554fs/+ background results in 23% or 15% respectively of the embryos having germ band retraction defects.

When EcRB1-ΔC655.F645A.Scer\UAS is driven by Scer\GAL4GMR.PF massive necrosis is seen in the eye, resulting in a collapse of the domed shape of the eye, a large decrease in the level of pigmentation. poorly defined facets and a very characteristic scar.

When EcRB1-ΔC655.F645A.Scer\UAS is driven by Scer\GAL4GMR.PF defects are seen in eye differentiation and a marked lethality is seen before adult eclosion.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
NOT Enhanced by
Statement
Reference
Suppressed by
NOT suppressed by
Statement
Reference
Phenotype Manifest In
Enhanced by
Suppressed by
Additional Comments
Genetic Interactions
Statement
Reference

The presence of ab1D/+ reduces the frequency of incomplete border migration in animals expressing EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4slbo.2.6 to 34% of stage 10 egg chambers.

The deleterious effect on female lifespan of expression of EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4da.Switch.PT in the presence of RU486 is suppressed by ovoD1.

The frequency of abnormal dorsal appendages in embryos derived from females carrying EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4slbo.2.6 (23%) is increased if the females are also heterozygous for one of the following alleles: E(bx)ry122 (84%), E(bx)Nurf301-2 (70%), Iswi1 (76%), Iswi2 (45%) or Nurf-381 (69%).

The addition of trr+t12 or SmrBG01648 to EcRB1-ΔC655.F645A.Scer\UAS, Scer\GAL4GMR.PF animals causes a dramatic decrease in the level of necrosis and scarring and some improvement of the morphology of the facets.

The lethality seen in EcRB1-ΔC655.F645A.Scer\UAS, Scer\GAL4GMR.PF animals is enhanced by the addition of trr1/+ or trr3/+. The lethality and the EcRB1-ΔC655.F645A.Scer\UAS, Scer\GAL4GMR.PF eye phenotype is partially suppressed by trr+t12. The lethality and the EcRB1-ΔC655.F645A.Scer\UAS, Scer\GAL4GMR.PF eye phenotype is partially suppressed by SmrBG01648.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Rescued by
Comments

Co-expression of EcRA.Scer\UAS postpones larval lethality from the 1st instar to the 2nd/3rd instar transition, but results in little-to-no rescue of the Malpighian tubule phenotypes of EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4c42. Cuticle preparations of these larvae show molting defects.

Co-expression of EcRB1.Scer\UAS results in partial rescue of larval lethality, and significant rescue of the Malpighian tubule phenotypes of EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4c42.

Co-expression of EcRB2.Scer\UAS results in nearly complete rescue of larval lethality and Malpighian tubule phenotypes of EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4c42.

Expression of either EcRB2.Scer\UAS or EcRB2-E9K.Scer\UAS under the control of Scer\GAL4ETH.Switch in the presence of RU486 fully rescues the lethality and failure of ecdysis phenotypes seen in larvae expressing EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4ETH.Switch in the presence of RU486.

Expression of either EcRA.Scer\UAS or EcRB1.Scer\UAS under the control of Scer\GAL4ETH.Switch in the presence of RU486 partially rescues the lethality and failure of ecdysis phenotypes seen in larvae expressing EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4ETH.Switch in the presence of RU486.

Co-expression of EcRB2.Scer\UAS rescues the Malpighian tubule defects (reduction in diameter of the tubules and reduction in number and change in distribution of stellate cells) seen in larvae expressing EcRB1-ΔC655.F645A.Scer\UAS under the control of either Scer\GAL4tsh-c724 or Scer\GAL4c649.

Co-expression of EcRB1.Scer\UAS with EcRB1-ΔC655.F645A.Scer\UAS in C4da neurons, under the regulation of Scer\GAL4ppk.PG results in the complete rescue of EcRB1-ΔC655.F645A.Scer\UAS-related dendritic pruning defects in C4da neurons.

Co-expression of EcRB1.Scer\UAS with EcRB1-ΔC655.F645A.Scer\UAS in C4da neurons, under the regulation of Scer\GAL4ppk.1.9 results in the complete rescue of EcRB1-ΔC655.F645A.Scer\UAS-related dendritic pruning defects in C4da neurons.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
Comments
Comments

Encodes a dominant negative form of EcR.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Symbol Synonym
EcRB1-ΔC655.F645A.Scer\UAS
EcRB1-ΔC655.F645A.UAS
Name Synonyms
Secondary FlyBase IDs
    References (48)