FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\beat-Ia2
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General Information
Symbol
Dmel\beat-Ia2
Species
D. melanogaster
Name
FlyBase ID
FBal0030623
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
beat2
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

In-frame deletion (codons 111-136 are deleted).

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

An in-frame deletion of codons G111-I136 of beat-Ia.

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

Cells of the Bolwig's organs (BOs) form in homozygous embryos, but the morphology of the larval visual system (LVS) is severely disrupted and increased numbers of photoreceptor cells are apparent from the earliest stages of LVS development. Extra photoreceptor cells are seen both in the normal location of the BO clusters and dispersed between the two clusters. Embryos sometimes contain three BO's and, rarely, four BO clusters are seen. Migration of the BOs appears relatively normal in some embryos, but in others it is disrupted and the BO does not achieve its proper location even though head involution appears normal, or the BO is elongated.

Motor axons exit the CNS normally but then fail to branch and enter their muscle domains once in the periphery. The SNb fails to diverge from the ISN either completely (full bypass), 41% segments, or partially (partial bypass), 41% segments, the SNc fails to diverge in 82% segments.

Defective in navigation through a specific choice point during intersegmental nerve and segmental nerve b pathfinding. CNS axon pathfinding is normal.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

beat-Ia2/beat-Ia3 Rac1N17.Scer\UAS Scer\GAL4elav-C155 double mutant embryos exhibit additive, not synergistic effects on the ISNb full bypass phenotype.

In beat-Ia2/beat-Ia3 transheterozygotes the SNb fails to diverge from the ISN completely (full bypass) in 38% segments or partially (partial bypass) in 28% segments. The divergence defect can be suppressed by Fas2e76 (but not significantly suppressed by Fas2e86 or Fas2e93) and the SNc defect by ConFvex238.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Scer\GAL4elav-C155 mediated expression of beat-IaScer\UAS.cFa rescues the SNb divergence defect.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
References (6)