FB2025_01 , released February 20, 2025
Allele: Dmel\EgfrDN.UAS.cBa
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General Information
Symbol
Dmel\EgfrDN.UAS.cBa
Species
D. melanogaster
Name
dominant negative
FlyBase ID
FBal0090688
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-EGFRDN, UAS-Egfr-DN, UAS-dnEGFR, UAS-DN-Egfr, UAS-DNDER, UAS-EGFRDN, UAS-DERDN, EgfrDN, UAS-EgfrDN.B
Key Links
Nature of the Allele
Progenitor genotype
Carried in construct
Cytology
Description

A dominant negative form of Egfr, with a stop codon introduced 20 amino acids C-terminal to the transmembrane domain, is expressed under the control of UASt regulatory sequences.

Allele components
Component
Use(s)
Encoded product / tool
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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

adult cuticle & head capsule | dorsal, with Scer\GAL4c591

axon & mechanosensory neuron & adult head, with Scer\GAL4unspecified

axon & ocellus sensory structure, with Scer\GAL4sca-537.4

Detailed Description
Statement
Reference

Somatic clones expressing EgfrDN.UAS.cBa under the control of Scer\GAL4Tub.PU contain a smaller overall number of cells and intestinal stem cells in adult flies compared to controls, but maintain a wild-type ratio of stem cells/clone.

Adulthood-generated midgut clones expressing EgfrDN.UAS.cBa under the control of Scer\GAL4Tub.PU have significantly fewer cells, but insignificant changes in the number and proportion of intestinal stem cells, as compared to control clones.

Expressing EgfrDN.UAS.cBa under the double control of Scer\GAL4twi.2PE and Scer\GAL4how-24B leads to embryos showing severely decreased numbers of cardioblasts, namely of generic cardioblasts, leading to a lower generic CBs:ostial CBs ratio than the typical 4:2 ratio.

Expressing EgfrDN.UAS.cBa under the control of Scer\GAL4twi.2PE leads to embryos showing a significant decrease in the number of odd pericardial cells, although even pericardial cells are unaffected, as compared to controls.

Expression of EgfrDN.Scer\UAS.cBa under the control of either Scer\GAL4Ret.P2 or Scer\GAL4GMR84B12 results in frequent loss or reduction of the frontal nerve and disruption of the recurrent nerve.

Expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4C587 (in combination with Gal80[ts] to restrict expression to adulthood) leads to a substantial increase in the number of germline stem cells in the germinal proliferation center, as compared to controls.

Expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4repo.PL (and using tub-Gal80[ts] to restrict the expression to larval stages) result in significantly reduced axon wrapping index (proportion of axon clusters wrapped by wrapping glia) and many axons are wrapped in abnormally large fascicles, expression under Scer\GAL4nrv2.PS also reduces the wrapping index but the number of wrapping glial cells along the nerve is unchanged whereas the number of perineurial glial cells is robustly decreased in third instar larvae.

In wild-type larvae, subperineurial glial cells (SPGs) form autocellular contacts with pronounced septate junction, the length of these autocellular contacts is significantly reduced upon Scer\GAL4moody.SPG-driven (in SPGs) knock-down of vn.

Expression of EgfrDN.Scer\UAS.cBa under the control of either Scer\GAL4ato.3'FL or Scer\GAL4ato.5'EYE results in loss or delay in photoreceptor neurons recruitment in the developing eye disc. Expression under the Scer\GAL4ato.5'EYE3' driver has even stronger effect and leads to a severe failure in photoreceptor neuron recruitment.

Scer\GAL4btl.PS-mediated expression of EgfrDN.Scer\UAS.cBa results in shorter tracheal ganglionic branches.

Larvae expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4n-syb.PS show a significantly lower learning index compared to control larvae in an olfactory learning assay. These larvae show normal gustatory preference responses to fructose and to quinine and show normal olfactory responses to amyl acetate and to 1-octanol.

Expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4elav.Switch.PO for just 24 hours in late larval stages (using mifepristone to control the timing of expression) results in significantly reduced olfactory learning ability in larvae.

Larvae expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4ey-OK107 show a significantly lower learning index compared to control larvae in an olfactory learning assay.

Expression of EgfrDN.Scer\UAS.cBa in the general epidermis and epidermal stripes, under the control of Scer\GAL469B and Scer\GAL4ptc-559.1, results in bowed embryos with occasional dorsal holes or scabs. 100% of embryos expressing EgfrDN.Scer\UAS.cBa with Scer\GAL4ptc-559.1 exhibit a bowed phenotype and 10% have a dorsal hole or scab.

Expression of EgfrDN.Scer\UAS.cBa during dorsal closure, under the control of Scer\GAL4LE reslts in a bowed embryo phenotype in about a quarter of embryos. Bowed embryos and dorsal holes are also seen when EgfrDN.Scer\UAS.cBa is expressed in the amnioserosa, under the control of Scer\GAL4c381.

Expression of under the control of Scer\GAL4Dl-05151-G (and using tub-Gal80[ts] to limit the stage of expression) diminishes the increase in the rate of intestinal stem cell division normally observed in the adult midgut upon bacterial infection challenge. This effect is not seen when EgfrDN.Scer\UAS.cBa is expressed under the Scer\GAL4esg.PU driver (with tub-Gal80[ts]).

Flies expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL471B show complete loss of wing veins.

Expression of EgfrDN.Scer\UAS.cBa in the tracheal system under the control of Scer\GAL4btl.PS results in gas-filling defects in the terminal cells.

Male Scer\GAL4elav.PU>EgfrDN.Scer\UAS.cBa flies have an approximately 13% body weight decrease.

Flies expressing EgfrDN.Scer\UAS.cBa using Scer\GAL4Ilp2.PR show no alterations in the morphology and number of insulin producing cells compared to controls.

Expression of EgfrDN.Scer\UAS.cBa in insulin producing cells under the control of Scer\GAL4Ilp2.PR results in reduced body weight in males.

Expression of EgfrDN.Scer\UAS.cBa in stage 16 embryos, under the control of Scer\GAL4neur-GAL4-A101 results in the loss of vdaB in 75% of parasegments. There is no loss of v'ada. Examination of stage 12 embryos reveals that vdaB-loss is preceded by SOP1a loss in 78% of cases. SOP4a are not affected.

Expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4MD-638 causes the loss of wing veins and reduction in wing size.

Cells expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4HHLT are unable to become lamellocytes following wasp infestation.

Expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4HHLT reduces the increase in lamellocyte number seen following wasp infestation.

Induction of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4wg-IS650 during 0-30 hours after pupal formation blocks apoptosis and rearranges the wing margin cells. In addition, blocking ecdysone signalling results in overlap of the double-row hairs in the adult wing.

Expression of EgfrDN.Scer\UAS.cBa in intestinal stem cells (ISCs) driven by Scer\GAL4esg-NP5130 and Scer\GAL80ts.αTub84B does not significantly affect the number of ISCs in the gut. However, in sharp contrast to wild-type flies, Erwinia carotovora carotovora 15 (Ecc15) infection does not increase the number of intestinal mitotic cells.

Guts from flies expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4Myo31DF-NP0001 are almost double the length and half the width compared with the guts of wild-type flies. However, the total number of enterocytes is the same as it is in wild-type controls. The alteration in gut length correlates with changes in the shape of enterocytes. In contrast to wild-type enterocytes, the mutant enterocytes appear flattened and lack the extension of their apical domain. In addition, the distance between nuclei of neighbouring enterocytes (indicative of epithelial density) increases twofold in these flies and altered in its axis. This effect on cell shape is more pronounced in certain gut segments, particularly around the copper cell region which is normally composed of a highly polarised columnar-type epithelium and is folded within the abdomen. As a consequence, guts of flies expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4Myo31DF-NP0001 are long and thin in this region and lack their characteristic folding.

Flies expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4Myo31DF-NP0001 succumb within 48 hours after ingesting Erwinia carotovora carotovora 15 (Ecc15). This increased susceptibility is associated with a rupture in gut integrity, as indicated by the presence of bacteria in the hemolymph.

Guts of flies overexpressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4Myo31DF-NP0001 and Scer\GAL80ts.αTub84B shifted to the restrictive temperature for 4 to 5 days are initially of normal size. A significant increase in gut length is observed when flies are incubated for 3 weeks at the restrictive temperature.

Guts of flies overexpressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4Myo31DF-NP0001 and Scer\GAL80ts.αTub84B are 20% longer compared with guts wild-type flies 48 hours post-infection with Erwinia carotovora carotovora 15 (Ecc15).

Guts of flies expressing EgfrDN.Scer\UAS.cBa in enterocytes under the control of Scer\GAL4Myo31DF-NP0001 and Scer\GAL80ts.αTub84B shrink less upon infection with Erwinia carotovora carotovora 15 (Ecc15). After a recovery phase of 2 or 8 days, the guts are 25% longer than their wild-type counterparts.

In contrast to wild-type flies, cell blebbing, the multi-layering of enterocytes or loss of cells into the lumen of flies are not observed in flies expressing EgfrDN.Scer\UAS.cBa in enterocytes under the control of Scer\GAL4Myo31DF-NP0001 and Scer\GAL80ts.αTub84B. In sharp contrast to wild-type enterocytes, apoptotic enterocytes with fragmented nuclei are observed within the epithelium of flies expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4Myo31DF-NP0001 and Scer\GAL80ts.αTub84B.

Embryos expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4twi.PG show a decrease in the number of dorsolateral and lateral adult muscle precursor cells compared to wild type.

The cardiac function of flies expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4tin.CΔ4 and Scer\GAL80ts.αTub84B is normal at 18[o]C, but, compared with controls, it progressively deteriorates at 25[o]C as manifested by enlarged end-diastolic (EDD) and end-systolic dimensions (ESD). The EgfrDN.Scer\UAS.cBa-mediated effects on cardiac chamber size are reversible when EgfrDN.Scer\UAS.cBa expression is repressed by temperature shift.

Expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4CY2 abolishes the dorsal eggshell structures.

Expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4CY2 results in a ventralised eggshell.

Expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4dpp.3KK results in loss of wing veins.

Expression of EgfrDN.Scer\UAS.cBa in the anterior cells of the egg chamber, under the control of Scer\GAL455B, results in eggs with a single fused dorsal appendage or with a patch of dorsal appendage material.

Expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL41151 does not affect founder cell formation of patterning.

Expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4ems.HRE impairs filzkorper formation but does not affect stigmatophore formation. However, expression of this transgene under the control of Scer\GAL4salm-459.2 has the reciprocal effect; stigmatophore formation is impaired while filzkorper formation is unaffected.

Expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4CY2 results in eggs with strongly ventralised chorions. Expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4GMR.PF results in a severe rough eye phenotype. The rough eye phenotype caused by expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4GMR.PF is not suppressed by EgfrSOK2/+.

The number of macrochaetae/heminotum in animals expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4ap-md544 is - anterior+posterior notopleural: 1.61, presutural: 0.70, anterior supraalar: 0.50, posterior supraalar: 0, anterior postalar: 0, posterior postalar: 0, anterior+posterior dorsocentral: 0.78 and anterior+posterior scutellar: 1.55.

EgfrDN.Scer\UAS.cBa; Scer\GAL4Bx-MS1096 flies have small curved wings with vein truncations.

When expression is driven by Scer\GAL4ap-md544 most notum macrochaetae are removed, though microchaetae are unaffected.

Embryos expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4twi.PG show loss of VA2 muscle precursor cells (only 26% of hemisegments contain VA2 precursor cells).

Expression of EgfrDN.Scer\UAS.cBa can result in loss of sensory organs in the ocellar sensory system (OSS), unless raised at 17oC, which allows some differentiation of these neurons. In these conditions, some axon guidance defects are seen in OSS neurons. The most common alteration (in about 1/3 of animals) is bristle mechanosensory (BM) axons stalling in the epidermis. Alterations in Ocellar pioneer (OP) axon guidance are much less frequent.

Expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4Gsc-SNS1 results in suppression of the formation of the anterior most invagination fold in the stomatogastric nervous system anlage, without affecting the others, in stage 11 embryos.

When expressed under the control of Scer\GAL4c591, the ocelli and the ocellar bristles are deleted. However, most of the interocellar cuticle is retained.

Expression of EgfrDN.Scer\UAS.cBa driven by Scer\GAL4Bx-MS1096 deletes parts of dorsal veins L3, L5 and the distal portion of L4, reduces the width of the wing, and causes mis-alignment between dorsal and ventral components of the veins.

The ventral muscle founder cells are specified in embryos expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4twi.PB.

Many myofibres are missing from all muscle groups in embryos expressing EgfrDN.Scer\UAS.cBa under the control of both Scer\GAL4twi.PG and Scer\GAL4how-24B. The precursor of muscles DA1 is missing. Muscles DO1, LT2 and LT4, and the eve-expressing pericardial cell precursors form normally. Apoptosis within the mesoderm is significantly higher than in wild-type embryos. Embryos expressing EgfrDN.Scer\UAS.cBa under the control of both Scer\GAL4twi.PG and Scer\GAL4how-24B show a partial reduction in the development of muscles DA1 and VA2. This phenotype is suppressed by co-expression of EgfrScer\UAS.cBa. The P15 muscle precursor cell does not form in embryos expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4twi.PG. Embryos expressing rhoScer\UAS.cBa under the control of Scer\GAL4twi.PG show a marked overproduction of eve-positive mesodermal founder cells. This phenotype is partly suppressed if the embryos are also carrying EgfrDN.Scer\UAS.cBa.

Scer\GAL4sca-C253 mediated expression generates flies with reduced eyes. Females carrying Scer\GAL4T155 and EgfrDN.Scer\UAS.cBa lay partially to completely ventralised eggs.

External Data
Interactions
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NOT Enhanced by
NOT suppressed by
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Suppressor of
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NOT Suppressor of
Phenotype Manifest In
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NOT Enhanced by
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NOT suppressed by
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NOT Enhancer of
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NOT Suppressor of
Additional Comments
Genetic Interactions
Statement
Reference

The increased division of intestinal stem cells in the adult posterior midgut during normal homeostasis characteristic for Sulf1KO;Cherry/Sulf1ΔP1 mutants can be suppressed by expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4NP6267 (using tub-Gal80[ts] to limit the time of expression to adulthood).

Expression of EgfrDN.Scer\UAS.cBa in the midgut cell progenitors under the control of Scer\GAL4esg-NP5130 (limited to the adult stages using Scer\GAL80ts.αTub84B) suppresses the formation of tumors in the anterior midgut of Sox21a6 mutant flies.

Scer\GAL4btl.PS-mediated expression of EgfrDN.Scer\UAS.cBa suppresses the tracheal cyst phenotype of exp135 embryos.

Expression of taydsRNA.Scer\UAS does not modify the wing vein loss phenotype seen when EgfrDN.Scer\UAS.cBa is expressed under the control of Scer\GAL4MD-638.

Neuronal EgfrDN.Scer\UAS.cBa expression using Scer\GAL4elav.PU suppresses the CblGD12111-induced increase in body weight in males.

Expression of EgfrDN.Scer\UAS.cBa in insulin producing cells under the control of Scer\GAL4Ilp2.PR suppresses the CblGD12111-induced increase in body weight in males.

The wing phenotypes resulting from the expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4MD-638 are not modified by the co-expression of krzdsRNA.Scer\UAS.

Co-expression of EgfrDN.Scer\UAS.cBa blocks the epithelium renewal induced by upd3Scer\UAS.cMa-expression under the control of Scer\GAL4esg-NP5130 and Scer\GAL80ts.αTub84B.

Co-expression of EgfrDN.Scer\UAS.cBa blocks the extra ISC proliferation induced by domeScer\UAS.T:Avic\GFP-EGFP-expression under the control of Scer\GAL4esg-NP5130 and Scer\GAL80ts.αTub84B.

The dorsalised chorion phenotype caused by expression of Egfr::kek1KEΔCG.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4CY2 is completely suppressed by coexpression of EgfrDN.Scer\UAS.cBa.

Expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4ap-md544 partially suppresses the extra bristle phenotype seen in ed1X5/edslH8 flies. The number of macrochaetae/heminotum in animals expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4ap-md544 in a ed1X5/edslH8 background is - anterior+posterior notopleural: 2.15, presutural: 1.05, anterior supraalar: 0.80, posterior supraalar: 0, anterior postalar: 0.60, posterior postalar: 0, anterior+posterior dorsocentral: 1.30 and anterior+posterior scutellar: 2.25.

Co-expression of csw::Src64Bsrc90.Scer\UAS significantly suppresses the loss of VA2 muscle precursor cells seen in embryos expressing EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4twi.PG (71% of hemisegments have VA2 cells).

The addition of stetScer\UAS.cGa or rhoScer\UAS.cBa to EgfrDN.Scer\UAS.cBa, Scer\GAL4Bx-MS1096 flies gives a phenotype almost identical to that of EgfrDN.Scer\UAS.cBa, Scer\GAL4Bx-MS1096 flies alone.

Co-expression of EgfrDN.Scer\UAS.cBa and rhoScer\UAS.cBa driven by Scer\GAL4Bx-MS1096 in females has an almost identical phenotype to Scer\GAL4Bx-MS1096 driven EgfrDN.Scer\UAS.cBa expression alone. In males a stronger vein-loss phenotype is seen. This phenotype is not significantly affected by vnScer\UAS.cSa or SScer\UAS.cGb. Co-expression of EgfrDN.Scer\UAS.cBa, EgfrScer\UAS.cBa and rhoScer\UAS.cBa driven by Scer\GAL4Bx-MS1096 fully restores the rhoScer\UAS.cBa induced ectopic vein phenotype.

The partial reduction in the development of muscles DA1 and VA2 seen in embryos expressing EgfrDN.Scer\UAS.cBa under the control of both Scer\GAL4twi.PG and Scer\GAL4how-24B is suppressed by co-expression of SScer\UAS.cBa, and is dominantly enhanced by SIIN.

The phenotypes caused by expression of EgfrDN.Scer\UAS.cBa under the control of Scer\GAL4T155 are enhanced in a cswLE120 or csw6 mutant background.

The phenotypes caused by expression of Scer\GAL4T155 under the control of EgfrDN.Scer\UAS.cBa are enhanced in a cswLE120 or csw6 mutant background.

Xenogenetic Interactions
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Complementation and Rescue Data
Partially rescued by
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Stocks (2)
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Synonyms and Secondary IDs (3)
Reported As
Symbol Synonym
EgfrDN.Scer\UAS.cBa
EgfrDN.UAS.cBa
Name Synonyms
dominant negative
Secondary FlyBase IDs
    References (86)