FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\miraZZ176
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General Information
Symbol
Dmel\miraZZ176
Species
D. melanogaster
Name
FlyBase ID
FBal0082440
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
mirZZ176
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

Deletion of nucleotides 1581-1749, which results in a frameshift after amino acid residue 446 (the protein produced contains 14 novel amino acid residues, which are RTWPRRSPRSTTTS).

169 bp deletion that causes a frameshift followed immediately by a stop codon. This produces a truncated protein lacking the C-terminal 384 amino acids, including the pros binding domain.

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

A 169bp deletion causes a frameshift, followed by a stop codon

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 ( 1 )
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

The transplantation of miraZZ176 larval neuroblast clones into the abdomen of adult hosts causes tumor growth, with clones growing to 100 times their original size thereby severely damaging and displacing the host's organs. Although genome stability is not grossly affected shortly after transplantation, 40-day-old tumors show karyotype defects such as segmental aneuploidy. Additionally, 15-20% of cells within the tumors have supernumerary centrosomes and these cells tend to be hyperploid.

Mutant embryos have a variable phenotype in the NGB 6-4T lineage, showing reduced, normal or extra NGB 6-4T-derived glia. Neuronal progeny of the NGB 6-4T lineage are completely absent in 46% of hemisegments but may be normal in other hemisegments.

Axon tracts of embryos are grossly defective, longitudinal connectives are generally broken or severely reduced in width and commissures are partially or completely fused.

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

mira5A.Scer\UAS.T:Ivir\HA1 expression is not able to rescue embryonic lethality of miraZZ176 animals.

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

One of a group of six alleles isolated in the same screen.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (9)