FlyBase Allele Report: Dmel\Egfr[f5]

General Information

Symbol

Dmel\Egfr^f5

Species

D. melanogaster

Name

FlyBase ID

FBal0003533

Feature type

allele

Associated gene

Dmel\Egfr

Associated Insertion(s)

Carried in Construct

Also Known As

flb^2G31, top^2G31

Key Links

Genomic Maps

JBrowse

Allele class

hypomorphic allele - genetic evidence

amorphic allele - genetic evidence

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Schejter and Shilo, 1989)

hypomorphic allele - genetic evidence

(Clifford and Schupbach, 1989)

Mutagen

ethyl methanesulfonate

(Clifford and Schupbach, 1994, Clifford and Schupbach, 1989, Tearle and Nusslein-Volhard, 1987)

Progenitor genotype

Cytology

Description

Amino acid replacement: W186term.

(Clifford and Schupbach, 1994)

Nucleotide substitution: G926A.

(Clifford and Schupbach, 1994)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

2R:21,555,368..21,555,368 [+]

Nucleotide change:

G21555368A

Reported nucleotide change:

G926A

Amino acid change:

W186term | Egfr-PA; W235term | Egfr-PB

Reported amino acid change:

W186term

Comment:

TGG to TAG

(Clifford and Schupbach, 1994)

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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

abnormal neuroanatomy

(de Velasco et al., 2007)

lethal - all die during embryonic stage | recessive

(Clifford and Schupbach, 1994, Clifford and Schupbach, 1989, Schejter and Shilo, 1989)

some die during embryonic stage | recessive

(Clifford and Schupbach, 1994, Clifford and Schupbach, 1989, Schejter and Shilo, 1989)

Phenotype Manifest In

adult optic lobe

(Dumstrei et al., 1998)

brain

(de Velasco et al., 2007)

corpus cardiacum primordium

(De Velasco et al., 2004)

embryonic head

(Dumstrei et al., 2002)

embryonic head epidermis

(Dumstrei et al., 2002)

embryonic optic lobe primordium

(Dumstrei et al., 2002)

embryonic stomatogastric nervous system

(De Velasco et al., 2004)

head

(de Velasco et al., 2007)

ventral nerve cord primordium

(Dumstrei et al., 2002)

Detailed Description

Statement

Reference

In Egfr^f5 mutants, all tissues of the dorso-medial head are almost completely eliminated by cell death. Brain hemispheres are far removed from each other and connected by only a few axons.

(de Velasco et al., 2007)

Late stage mutant embryos show a strong reduction in size of the corpus cardiacum compared to wild type and the stomatogastric nervous system is absent.

(De Velasco et al., 2004)

Egfr^f5 stage 11 embryos show domains of cell death in the anterior and posterior parts of the head. The posterior domain covers the optic placode. The apoptosis results in loss of major portions of the head epidermis, so that the brain is exposed in stage 14 embryos. The optic placode has almost disappeared by stage 14. The apoptosis is delayed in the optic placode relative to the apoptosis in the head epidermis. Cell death is also seen in the ventral neuroectoderm at stage 10/11.

(Dumstrei et al., 2002)

In mutant embryos, massive cell death occurs in the head. The visual system is almost entirely absent, though the Bolwig's organ remains.

(Dumstrei et al., 1998)

Enhances the female sterility and adult morphological defects of Egfr^t1. Rarely survives as transheterozygote with the semi-viable Egfr^top-CA allele.

(Clifford and Schupbach, 1994)

Homozygotes and hemizygotes display an intermediate 'flb' phenotype. Embryos produced from heteroallelic combination with Egfr^t1 have a severe ventralised phenotype, reduction in size of their dorsal appendage.

(Clifford and Schupbach, 1989)

severe allele

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Phenotype Manifest In

Suppressed by

Statement

Reference

Egfr^f5 has adult optic lobe phenotype, suppressible by Df(3L)H99

(Dumstrei et al., 1998)

NOT suppressed by

Statement

Reference

Egfr^f5 has phenotype, non-suppressible by eRF1[+]/eRF1^F2

(Chao et al., 2003)

Suppressor of

Statement

Reference

Egfr^f5 is a suppressor | partially of eye phenotype of Krn^UAS.cRa, Scer\GAL4^GMR.PF

(Reich and Shilo, 2002)

Egfr^f5 is a suppressor | partially of ommatidium phenotype of Krn^UAS.cRa, Scer\GAL4^GMR.PF

(Reich and Shilo, 2002)

Other

Statement

Reference

Df(3L)H99, Egfr^f5 has embryonic optic lobe primordium phenotype

(Dumstrei et al., 2002)

Df(3L)H99, Egfr^f5 has Bolwig organ primordium phenotype

(Dumstrei et al., 2002)

Additional Comments

Genetic Interactions

Statement

Reference

The optic placode fails to invaginate in Egfr^f5 ; Df(3L)H99 embryos, leaving it exposed at the surface of the embryo. Cells that would normally separate from the placode and become the Bolwig's organ remain part of the placode. These cells show a typical epithelial phenotype and are structurally indistinguishable from the surrounding optic lobe cells (although they express neuronal markers). In some cases, outgrowth of short, axon-like processes is seen.

(Dumstrei et al., 2002)

The optic lobes are restored in double mutants with Df(3L)H99.

(Dumstrei et al., 1998)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Comments

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

34504

cn¹ Egfr^f5 bw¹ speck¹/CyO

Notes on Origin

Discoverer

Selected as: Embryonic lethal.

Comments

Mutation of Egfr that coordinately affects all gene activities, a class I lesion. The allelic series for class I lesions: Egfr^t2 = Egfr^t1 < Egfr^top-EC20 < Egfr^f7 = Egfr^f1 = Egfr^flb-2E07 < Egfr^top-EE39 = Egfr^top-ED26 = Egfr^f5 < Egfr^f9 = Egfr^f10 = Egfr^f2 = Egfr^top-EE42 = Egfr^f11 = Egfr^f24 = Egfr^f3 = Df(2R)Egfr3.

(Clifford and Schupbach, 1989)

Double mutants for Egfr and sdt or crb show an enhancement of the sdt or crb mutant phenotype.

(Tepass and Knust, 1993)

Class I allele.

(Clifford and Schupbach, 1994)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (7)

Reported As

Symbol Synonym

Egfr¹⁵

(de Velasco et al., 2007)

Egfr^f5

flb

flb^2G31

(de Velasco et al., 2007, De Velasco et al., 2004, Chang et al., 2003, Reich and Shilo, 2002, Raz et al., 1991, Schejter and Shilo, 1989)

flb^IIG

(Tearle and Nusslein-Volhard, 1987)

top^2G31

(Clifford and Schupbach, 1994, Clifford and Schupbach, 1989)

Name Synonyms

faint little ball

Secondary FlyBase IDs

References (15)

Report Sections

Open Close