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General Information
Symbol
Dmel\BicD2
Species
D. melanogaster
Name
FlyBase ID
FBal0001141
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Bic-DIIIE48, BicDIIIE, BicDIIIE48, BicDEIII48
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

G17464050A

Reported nucleotide change:

G?A

Amino acid change:

E224K | BicD-PA; E224K | BicD-PB; E224K | BicD-PC; E224K | BicD-PD

Reported amino acid change:

E224K

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

Nucleotide substitution: GAG to AAG Amino acid replacement: E224K.

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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Embryos derived from BicD1/BicD2 mothers show a duplication of posterior structures and a lack of anterior structures. These embryos lack macrophages. Apoptotic cells accumulate at the ventral surface of the central nervous system (CNS), and subperineural glia contain an abundance of apoptotic cells. Single unengulfed apoptotic cells are also seen inside the CNS. The number of subperineural glia per abdominal segment is not significantly different from wild-type in stage 16 embryos.

Does not prevent the posterior localization of G-iα65A protein.

Ectopic nos activity at the anterior pole of embryos derived from BicD2 mutant females blocks bcd protein expression from bcdΔ transcripts but not from bcd+ transcripts. None of the embryos bearing the bcdΔ mRNA display the bcd phenotype.

Heterozygous embryos have duplicated posterior poles, lack polar granules and do not form pole cells. No CycB transcript accumulation was seen at the posterior pole.

Lack of head and thoracic anlagen is caused by the lack of bcd protein.

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
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments

Does not interact with RpII140wimp maternal effect.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (24)