FB2026_02 , released June 18, 2026
Allele: Dmel\nerfin-154
Open Close
General Information
Symbol
Dmel\nerfin-154
Species
D. melanogaster
Name
FlyBase ID
FBal0175567
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description

A deletion removes a 2347bp segment that includes the minimal promoter and 5' transcribed leader sequence.

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

In mutant embryos, most embryos within longitudinal connectives fail to project across segmental boundaries and frequently terminate in tangles at or near the boundaries. In addition, both the anterior and posterior commissures of each segment fail to develop properly. Also the overall fascicle organisation and apparent axon density of the ventral commissures is affected. The motor neuron nerve tracts and the axon patterning of the peripheral nervous system appears normal. In mutant embryos the pCC interneurons fail to send their axons anteriorly and instead project their axons either in a lateral or posterior direction, and any of the posterior projecting pCC axons cross the ventral midline in adjacent posterior segments. By stage 14, all pCC interneurons have misguided axons and many of these axons have extensive side branches. The overall development and patterning of the aCC and RP2 motorneuron axon tracts do not appear to be adversely affected.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Enhanced by
Statement
Reference
Enhancer of
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
Comments
Comments

Created as a consequence of the "ends in" homologous recombination gene knockout technique. The deletion was most likely caused by exonuclease digestion of the targeting vector after the SceI exonuclease induced double strand break but before its integration into the nerfin-1 chromosomal locus. The deletion was detected after the allelic substitution step and are most likely the result of illegitimate recombination between micro-homologies present in the minimal promoter of one copy of the nerfin-1 duplication and the transcribed region of the tandem copy.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
Reported As
Symbol Synonym
Df(3L)nerfin-154
nerfin-1null
nerfin-1Δ54
Name Synonyms
Secondary FlyBase IDs
    References (4)