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General Information
Symbol
Dmel\BicDR26
Species
D. melanogaster
Name
FlyBase ID
FBal0001144
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Bic-DR26
Key Links
Mutagen
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Comment:

A deletion of 12 nucleotides which removes amino acids 376-379. This is in addition to the F684I mutation of the parental BicD[1] chromosome.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Cytology
Nature of the lesion
Statement
Reference

Deletion of amino acids 376-379.

Deletion of 12 nucleotides.

sequenced by Suter and Steward, 1991 deletion of residues 376-379 superimposed on BicD1 lesion

Expression Data
Reporter Expression
No Assay Recorded
Stage
Tissue/Position (including subcellular localization)
Reference
in situ
Stage
Tissue/Position (including subcellular localization)
Reference
Additional Information
Statement
Reference

BicDR26 protein becomes localized to the oocyte at significantly higher levels than in wild type.

In wild type females, BicD RNA is detected very early in oogenesis in the 16 cystocyte cluster and progressively accumulates in a single cell, the oocyte. In BicDR26 mutants, BicD RNA does not localized to a single cystocyte, but is found in all of the pro-nurse cells.

 
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

13% of neuroblast mitoses are more than 45o off-axis in embryos derived from BicDHA40.T:Ivir\HA1 ; BicDR26/Df(2L)TW119 females mated to BicDR26/+ males (in contrast to wild type where all neuroblast divisions are oriented within 45o of the apicobasal axis). The average length of metaphase spindles in these mutant neuroblasts is significantly less than normal.

Mutant ovaries fail to make an oocyte.

More than 4 cells per germline cyst enter meiosis in homozygous females, but the cysts still retain a graded distribution of the synaptonemal complex (SC), with the highest levels in the two pro-oocytes. The SC sometimes becomes restricted to these 2 cells in region 2b/3, but eventually disappears in region 3. The 2 cells eventually adopt the nurse cell fate.

When in combination with BicDH2, BicDH3 or BicDHA40.T:Ivir\HA1 over null or loss of function BicD, BicDR26 increases the proportion of ventralised eggs to 100%. When transheterozygous with a wild type allele, female fertility is normal.

Fusomes in the cysts of BicDr/BicDR26 ovaries appear to form normally.

Egg chambers of hemizygous females start to degenerate around stage 7.

Embryos exhibit a fused dorsal appendage.

No oocyte differentiation, no microtubule organising centre.

Fusomes are normal.

No single microtubule organizing center forms in the germaria of hemizygous females, instead several small foci are present. The actin cytoskeleton is unaffected.

Abdominal defect: no eggs.

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

BicDR26 has phenotype, suppressible by kst01318

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

Revertant.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (38)