FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\domeG0217
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General Information
Symbol
Dmel\domeG0217
Species
D. melanogaster
Name
FlyBase ID
FBal0126402
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dome217
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Associated Insertion(s)
Cytology
Description

The P{lacW} insertion is at nucleotide +168 of the 4.8kb dome transcript.

P{lacW} insertion in the 5' UTR, at nucleotide position 154 of dome EST LD32858.

Insertion of P{lacW} into 5' UTR of dome, at position of 154bp with respect to the start of LD32858.

Allele components
Component
Use(s)
Inserted element
Encoded product / tool
Mutations Mapped to the Genome
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

domeG0217 mutants show premature differentiation to P1+ plasmatocytes.

Mutant animals are lethal at the first instar larval stage and show a phenotype in the gastrointestinal tract indicate by a block of food passage at the defective proventriculus organ. A failure of ectodermal cells to invaginate and a disorganised endodermal layer of the proventriculus is seen. The proventriculus development is normal in early stages of proventriculus development in mutants. However in the keyhole stage, the anterior boundary cells fail to move inward into the endodermal keyhole domain and arrest anterior to the proventricular endoderm until late stages of embryonic development. Furthermore, the endodermal cell layer of the keyhole is disorganised and the proventriculus is collapsed.

Homozygous embryos lack filzkorper.

Lethality occurs during the embryonic stage and the first larval instar.

The shape of the posterior spiracles is affected in mutants. Homozygous embryos derived from homozygous female germline clones have segmentation defects, such as deletion of segment A5 and most of the A4 denticle belts, partial or total fusion of segments A6 and A7 and a variable reduction of the thoracic segments and A8.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

The enlarged eye phenotype seen in flies carrying one copy of upd1GMR.PB is moderately suppressed by one copy of domeG0217.

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

Mobilisation of the P-element reverts both the lethality and posterior spiracle phenotype.

External Crossreferences and Linkouts ( 1 )
Crossreferences
GenBank Nucleotide - A collection of sequences from several sources, including GenBank, RefSeq, TPA, and PDB.
Synonyms and Secondary IDs (4)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (8)