FB2026_02 , released June 18, 2026
Allele: Dmel\slmb00295
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General Information
Symbol
Dmel\slmb00295
Species
D. melanogaster
Name
FlyBase ID
FBal0083748
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
slimbP1493, slimbP, l(3)00295
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Associated Insertion(s)
Cytology
Description

P{PZ} insertion 182 nucleotides upstream of the ATG.

Insertion of P{PZ} into the first exon of slmb.

Allele components
Component
Use(s)
Inserted element
Encoded product / tool
Mutations Mapped to the Genome
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 ( 1 )
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

slmb00295 mutant C4da neuron clones exhibit an increase in cell death and die during early metamorphosis.

No defects are seen in axon pruning during metamorphosis.

Homozygotes carrying a single copy of slmbαTub84B.PJ are viable and show normal morphology, 5-10% of adults exhibit duplication of the haltere. Mutant cells undergo only a few divisions and show phenotypes characteristic of ectopic wg and hh signal transduction. Clones in the wing cause generation of ectopic sensory bristles along the wing margin, instead of epidermal hairs. Heterozygotes with slmb1 die as pupae and heterozygotes with slmb2 die during early larval life.

Clones of mutant cells in the leg and wing discs cause outgrowths of slmb+ cells and pattern disruptions including duplicated structures. Outgrowths occur both ventrally and dorsally and both anteriorly and posteriorly.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Suppressed by
Statement
Reference

ago3, slmb00295 has glial cell | embryonic stage phenotype, suppressible by gcmN7-4/gcm[+]

ago3, slmb00295 has glial cell | embryonic stage phenotype, suppressible by gcm26

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

slmb00295, ago3 double mutant embryos display a disrupted glial pattern compared to single mutant or control embryos. An increase in repo-positive glial cell number is observed. An increase in cell proliferation is observed, and no increase in cell death is seen.

Expression of slmbαTub84B.T:Hsap\MYC in slmb00295, ago3 double mutant embryos significantly suppresses the increased number of glial cells observed in the slmb00295, ago3 mutant embryos.

slmb00295, ago3, gcmN7-4 triple mutants results in the absence of almost all glia, as observed in gcmN7-4 single mutants. One copy of gcmN7-4 suppresses the increased glial cell number phenotype observed in slmb00295, ago3 double mutants.

gcm26 suppresses the increased glial cell number phenotype observed in slmb00295, ago3 double mutants.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer

A. Spradling.

Comments
Comments

Previously assigned as an allele of Atpα in FlyBase (in error). Now known to be an allele of slmb, based on the insertion of the P{PZ} element within the slmb transcription unit, reversion of the mutant phenotype by precise excision of the P{PZ} insertion and rescue of the mutant phenotype by a transgene containing the slmb coding region (see FBrf0100581 and FBrf0104785).

Wild type slmb function can be restored by precise excision of the P{PZ} insertion.

Complements: Atpα01453a. Complements: ppan02231. Complements: Atpα07008. Complements: rtet07086. Complements: Atpα07097. Complements: ppanj6B6. Complements: l(3)neo541.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (10)
References (24)