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General Information
Symbol
Dmel\BicD1
Species
D. melanogaster
Name
FlyBase ID
FBal0001140
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
BicD7134, Bic-D71.34, BicD71.34
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

T17462435A

Reported nucleotide change:

T?A

Amino acid change:

F684I | BicD-PA; F684I | BicD-PB; F684I | BicD-PC; F684I | BicD-PD

Reported amino acid change:

F684I

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

Nucleotide substitution: TTC to ATC Amino acid replacement: F684I.

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

BicD1/BicDr5 females show reduced enrichment of yolk granules at the posterior of stage 8-9 oocytes compared to wild type.

Heterozygous BicD1 females produce 16% wild-type embryos and 84% embryos with various defects, including reduced mouthparts and bicaudal phenotypes.

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.

Embryos from mutant females are bicaudal.

Hemocytes cannot be detected, suggesting that in the absence of head mesoderm the trunk population of mesoderm cannot produce hemocytes. Cellular debris becomes located in the extracellular space.

Ectopic nos activity at the anterior pole of embryos derived from BicD1 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.

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
Suppressed by
Statement
Reference

BicD1 has embryo phenotype, suppressible by pAbp[+]/pAbpk10109

BicD1 has embryo phenotype, suppressible by pAbp37-2/pAbp[+]

BicD1, pAbp[+]/pAbpk10109 has embryo phenotype, suppressible by pAbp+t7.8

BicD1, pAbp37-2/pAbp[+] has embryo phenotype, suppressible by pAbp+t7.8

Additional Comments
Genetic Interactions
Statement
Reference

The BicD1/+ mutant embryonic phenotypes are suppressed by pAbpk10109/+.

The BicD1/+ mutant embryonic phenotypes are suppressed by pAbp37-2/+.

The suppression of the BicD1/+ embryonic phenotypes by pAbpk10109/+ is partially reverted by one copy of pAbp+t7.8.

The suppression of the BicD1/+ embryonic phenotypes by pAbp37-2/+ is partially reverted by one copy of pAbp+t7.8.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (5)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (8)
References (31)