FB2024_03 , released June 25, 2024
Allele: Dmel\Egfrtop-101
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General Information
Symbol
Dmel\Egfrtop-101
Species
D. melanogaster
Name
FlyBase ID
FBal0029753
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
top101
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

Nucleotide substitution: C3666T. Amino acid replacement: P1054S.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Nucleotide change:

C21558108T

Reported nucleotide change:

C3666T

Amino acid change:

P1054S | Egfr-PA; P1103S | Egfr-PB

Reported amino acid change:

P1054S

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
Detailed Description
Statement
Reference

Malpighian tubules in homozygous embryos are shorter than wild type, posterior tubules are more strongly affected than the anterior. Reduction in size of the tubules is due to reduction in cell number, not cell death.

Homozygotes show a weak Egfr phenotype: the cuticle is more intact than in stronger Egfr alleles, but shows reductions in the ventral plate and H piece of the anterior head skeleton. There are variable reductions in the number and size of ventral setae and occasional ventral or dorsal midline defects. Many embryos fail to complete germ band retraction.

Weak 'flb' phenotype when homozygous and hemizygous. Embryos produced from heteroallelic combination with Egfrt1 have a severe ventralised phenotype, reduction in size of their dorsal appendage. Individuals are fully viable over the pupal lethals Egfrtop-CA and Egfrtop-EC20 and show a reduction in viability over Egfrtop-EB.

Head skeleton is defective, germ band fails to retract and abdominal denticle belts are reduced in width.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Suppressor of
Statement
Reference

Egfrtop-101 is a suppressor of phenotype of rhohs.sev

Additional Comments
Genetic Interactions
Statement
Reference
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
Comments
Comments

Mutation of Egfr that affects the gene function required for embryogenesis, a class II lesion. The allelic series for class II lesions: Egfrtop-101 < Egfrtop-JE14 = Egfrf4 < Egfrf6.

Germline clone analysis indicates that there is very little, if any, requirement for Egfr in the germline.

Weak mutation.

Class IIA allele. Class IIA alleles do not disrupt tissue specific gene functions. Class II alleles fully or partially complement the developmental defects of Egfrt1 and Egfrtop-CA. Substantially complements the postembryonic lethality of Egfrtop-EC20. Several combinations of Egfr alleles involving Egfrtop-101, Egfrf4, Egfrf8 and Egfrf6 demonstrate interallelic complementation.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (8)