FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\obe2
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General Information
Symbol
Dmel\obe2
Species
D. melanogaster
Name
FlyBase ID
FBal0318086
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Mutagen
Nature of the Allele
Progenitor genotype
Cytology
Description

19bp deletion in the second obe exon and a C173T point mutation. These changes introduce a frameshift after amino acid 48 and a stop codon at amino acid 52.

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

19 base deletion in the second exon of obe which causes a frameshift. One of two lesions in mutant.

Nucleotide change:

C15486369T

Reported nucleotide change:

C173T

Amino acid change:

P58L | obe-PA

Comment:

A single base change causing a stop codon in the mutant (in the context of the 19 bp frameshift-inducing deletion just upstream also found in the @obe[2] mutant). There is also a C to T polymorphism between the reported sequence and the reference genome sequence 8 bases upstream of this point mutation.

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

Embryos derived from obe1/obe2 females show significantly reduced axis elongation during germband extension compared to wild type (the severity of the defect is unaffected by the paternal obe contribution).

obe2/Df(3R)Exel6174 embryos derived from obe2/Df(3R)Exel6174 females crossed to obe2/+ males show significantly reduced axis elongation during germband extension compared to wild type.

obe2/Df(3R)Exel6174 embryos derived from obe2/Df(3R)Exel6174 females crossed to obe2/+ males and obe1/obe2 embryos derived from obe1/obe2 females crossed to obe2/+ males show an abnormal aggregation of adherens junction proteins at stage 7.

In contrast to wild type, most of the centrosomes in epithelial cells fail to dissociate from microtubules and remain in close proximity to adherens junctions throughout axis elongation (stages 6 and 7) in obe1/obe2 embryos derived from obe1/obe2 females crossed to obe2/+ males. This results in a failure of the centrosomes to relocalise laterally. The mis-positioned centrosomes are often associated with adherens junction aggregates.

The adherens junction and centrosome defects seen in stage 7 obe1/obe2 embryos derived from obe1/obe2 females crossed to obe2/+ males are rescued by nocodazole treatment (which inhibits microtubule polymerisation).

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

Expression of obeCH322-15H13 rescues the axis elongation defects seen during germband extension in the progeny of obe1/obe1 and obe1/obe2 females crossed to obe1/+ males.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer

Separable mutation isolated in the P{XP}Surf4d04274 insertion line.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (1)