FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\D3
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General Information
Symbol
Dmel\D3
Species
D. melanogaster
Name
FlyBase ID
FBal0002211
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Mutagen
Nature of the Allele
Caused by aberration
Cytology
Description

The D3 allele is a partial revertant of D1. It retains the inversion; however it has suffered an additional DNA lesion within the coding sequence of the D transcription unit.

Deletion of the 3' portion of the D transcription unit. Protein null when assayed in whole mount embryos with anti-D antisera.

Breaks in 3' D regulatory sequences.

Shares the D1 breakpoint as well as an additional DNA lesion within 1kb of the 3' end of the D transcription unit.

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
Detailed Description
Statement
Reference

Viability of transheterozygotes is as follows: D3/D89 - 2.7%, D3/D107 - 14.4%, D3/D175 - 6.4%.

In stage 16 D3/Df(3L)fz-GS1a mutant embryos, the cells of the large intestine are short and rounded in contrast to the thin columnar cells of wild-type.

Behaves as a null allele when assayed in the embryo.

Lethal in combination with point alleles of D and small deletions which only remove D sequences.

80% of hemizygous embryos have severe defects throughout the nerve cord, showing thinning of longitudinal connectives and fusion of commissures. The remaining midline glia cells are more frequently located anterior to the anterior commissure than in wild-type embryos. The cell bodies of the midline glia lie along the ventral surface of the commissures and do not migrate and ensheath the commissures.

In(3L)D3/Df(3L)D-5rv6 embryos exhibit variable segmentation defects. Severe phenotype involves deletions removing half of the segments, intermediate phenotype involves weaker partial deletions and segment fusions, weak phenotype causes naked cuticle in segments A2 and A8. Embryos also exhibit variable defects in head development.

Partial revertant of the dominant phenotypes of D1. D3 is lethal over both "Sai" alleles of mirr but other D alleles are viable with these alleles. Wings held out at 80o but often a nubbin of alula is present, halteres are at partially held down, thorax and head are normal.

Less extreme than D1. Wings extended and lifted; alulae missing. Heat effect of D1 missing. Bristles usually wild type; occasionally outer verticals, upper humerals, presuturals, and anterior postalars absent. Viability of D3/+ better than D1/+. RK2A.

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

D3/Df(3L)fz-GS1a has larval hindgut & embryo & cell phenotype, suppressible | partially by dppUAS.cSa/Scer\GAL4en-e16E

Additional Comments
Genetic Interactions
Statement
Reference

When dppScer\UAS.cSa is expressed under the control of Scer\GAL4en-e16E in D3/Df(3L)fz-GS1a embryos, significant, though variable rescue of the D3/Df(3L)fz-GS1a hindgut phenotype is seen.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (5)
Notes on Origin
Discoverer

Plunkett, June 1924.

It is possible that the D1 and D3 inversions reflect dominant mutations in the 'Sail' function of mirr (see mirrSaiD1 and mirrSaiD3).

Revertant \partial.

Comments
Comments

Shows tissue specific loss of D expression in the embryo.

There is some uncertainty in the designation of D1, D3 and "D9" as dominant D alleles. The wing phenotype of D3 (a protein null) is similar, if not identical, to D1 when assayed in outcrossed individuals; it is thus possible that the phenotype of D1 itself is not due to changes at the D locus.

Associated with a recessive lethal phenotype that maps to 70D1-2.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
  • FBal0032088
References (12)