FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\ovoD3
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General Information
Symbol
Dmel\ovoD3
Species
D. melanogaster
Name
FlyBase ID
FBal0013377
Feature type
allele
Associated gene
Dmel\ovo
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class

antimorphic allele - genetic evidence

Mutagen
Nature of the Allele
Allele class

antimorphic allele - genetic evidence

(Mevel-Ninio et al., 1996, Chou et al., 1993, Lindsley and Zimm, 1992, Wei et al., 1991, Oliver et al., 1990)
Mutagen
ethyl methanesulfonate
(Lindsley and Zimm, 1992)
Progenitor genotype
Cytology
Description

Mutation creates a new in-frame AUG codon in the open reading frame in exon 2.

(Mevel-Ninio et al., 1996)

Nucleotide substitution: A1336T.

(Mevel-Ninio et al., 1996)

Amino acid replacement: K97M.

(Mevel-Ninio et al., 1996)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
point_mutation
X:5,064,717..5,064,717 [+]
Nucleotide change:

A5064717T

Reported nucleotide change:

A1336T

Amino acid change:

K226M | ovo-PB; K97M | ovo-PC; K226M | ovo-PE

Reported amino acid change:

K97M

(Mevel-Ninio et al., 1996)
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
      Phenotype Manifest In
      Detailed Description
      Statement
      Reference

      ovoD3/+ females carrying ovoD1r+ produce embryos, but they die before hatching with gross and variable defects in cuticle differentiation including holes, especially anteriorly, segment deletions and fusions, failed head involution and deletions of anterior elements of the mouthparts.

      (Andrews et al., 2000)

      Females carrying ovoD3 in an ovo-/+ background show dominant female sterility. The eggs produced by these females are flaccid and have chorion defects such as fused dorsal appendages.

      (Andrews et al., 1998)

      The dominant ovoD3 phenotype is significantly enhanced by one copy of Df(2R)vg135, Df(2R)stil-A or Df(2R)stil-B.

      (Pennetta and Pauli, 1997)

      In heterozygous females oogenesis is arrested.

      (Mevel-Ninio et al., 1996)

      Affect is weaker than for ovoD2. ovoD3/+ females produce many eggs that look almost normal except for the permeability of the membrane and frequent fusion of their dorsal appendages.

      (Pauli et al., 1995)

      Oogenesis is nearly normal in heterozygous females.

      (Granadino et al., 1992)

      Permeable eggs.

      (Lindsley and Zimm, 1992)

      Heterozygous females develop normally and can lay eggs although they are flaccid and degenerate.

      (Mevel-Ninio et al., 1991)

      Ovaries usually contain many late stage eggs. Fertility is restored by the presence of two copies of ovo+.

      (Wei et al., 1991)

      Most of the egg chambers of heterozygous females develop into eggs that are laid (more than 30% of the wild-type number of eggs are laid per day). The eggs are usually permeable to neutral red and have fused dorsal appendages. The soma is wild-type. Transheterozygotes with either ovoM1, ovoM2 or ovoD1rv20 have germ cells resembling early spermatocytes.

      (Oliver et al., 1990)

      Mutant gene activity works in opposition to wild type activity. Viable. Male germ line is fertile, female germ line has permeable eggs.

      (Oliver et al., 1987)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Phenotype Manifest In
      Additional Comments
      Genetic Interactions
      Statement
      Reference
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Comments

      This maternal effect lethality can be rescued by ovoΔa2, ovoamk or ovoΔap.

      (Andrews et al., 2000)
      Images (0)
      Mutant
      Wild-type
      Stocks (1)
      Notes on Origin
      Discoverer

      Komitopoulou.

      (Lindsley and Zimm, 1992)
      Comments
      Comments

      The dominant ovoD3 mutation has been reverted to a recessive loss of function mutation by insertion of a copia element.

      (Mevel-Ninio et al., 1991)

      Partially suppresses the female-specific gonadal dysgenesis caused by hybrid dysgenesis at 27.5oC.

      (Wei et al., 1991)

      Shows a dominant interaction with otu alleles: more extreme mutant phenotype as assayed by reduction in number of egg chambers at stage 10 or further developed.

      (Pauli et al., 1993)

      Parental strain: fs(1)N.

      (Mevel-Ninio et al., 1996)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (2)
      Reported As
      Symbol Synonym
      fs(1)K155
      (Lindsley and Zimm, 1992)
      ovoD3
      (Popodi et al., 2010-)
      Name Synonyms
      Secondary FlyBase IDs
        References (19)