FB2026_02 , released June 18, 2026
Allele: Dmel\sni1
Open Close
General Information
Symbol
Dmel\sni1
Species
D. melanogaster
Name
FlyBase ID
FBal0158627
Feature type
allele
Associated gene
Dmel\sni
Associated Insertion(s)
P{lacW}sni1
Carried in Construct
Key Links
Allele class

hypomorphic allele - genetic evidence

Mutagen
Nature of the Allele
Allele class

hypomorphic allele - genetic evidence

(Botella et al., 2004)
Mutagen
P-element activity
(Botella et al., 2004)
Progenitor genotype
Associated Insertion(s)
P{lacW}sni1
Cytology
Description

The P{lacW}sni1 insertion maps within the first intron of sni and also within an exon of one of the two 5' UTRs of Trxr-1 (overlapping genes on opposite strands).

(Botella et al., 2004)
Allele components
Component
Use(s)
Inserted element
P{lacW}
Encoded product / tool
lacZ
Tagged with
Tag:NLS(P)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
      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
      model of  neurodegenerative disease
      CEA
      (Krishnan et al., 2012)
      Modifiers Based on Experimental Evidence ( 1 )
      Disease
      Interaction
      References
      model of  neurodegenerative disease
      is exacerbated by per01
      (Krishnan et al., 2012)
      Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
       
      Disease-implicated variant(s)
       
      Phenotypic Data
      Phenotypic Class
      Phenotype Manifest In
      Detailed Description
      Statement
      Reference

      sni1 mutants do not display any significant difference in life span as compared to controls when reared in 12h light, 12h dark cycles, but exhibit significantly decreased lifespan when reared in constant light; sni1 mutants exhibit evidence of neurodegeneration, with vacuoles present in 9 day-old male brains and increasing in number in 19 day-old male brains, and vacuolization worsens when reared in constant light; climbing ability of sni1 mutants is modestly but significantly impaired; a subset of sni1 mutants display loss of circadian rhythm.

      (Krishnan et al., 2012)

      Mutant flies show age-related neurodegeneration; adults show significant vacuolisation of the cortex and neuropil in the brain which increases with age. Vacuolisation of the neuropils correlates with apoptosis of neurons in the corresponding cortex areas. 5 day old mutant flies have an intact set of lamina monopolar neurons that are surrounded by glia. By 15 days after eclosion, the mutant flies show the typical morphology of apoptosis in both neurons and glial cells of the lamina cortex. At 25 days after eclosion, few groups of lamina monopolar neurons are intact and an increased number of apoptotic bodies are seen. Hyperoxia treatment for 4 days enhances the brain degeneration phenotype of 7 day old mutant flies. Mutant flies have a reduced lifespan under normal oxygen conditions compared to wild-type flies. Under hyperoxia (99.5% oxygen), the mean and maximum lifespan of sni1 flies is reduced by 76.6% and 33% respectively, suggesting a hypersensitive response to hyperoxia. Mutant flies have a sluggish walking phenotype that deteriorates with age. 1 day old mutant flies already show an impaired ability to perform in the negative geotaxis paradigm.

      (Botella et al., 2004)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Enhanced by
      Statement
      Reference

      sni1 has abnormal neuroanatomy | progressive phenotype, enhanceable by per01

      (Krishnan et al., 2012)

      sni1 has abnormal locomotor behavior | adult stage phenotype, enhanceable by per01

      (Krishnan et al., 2012)
      NOT Enhanced by
      Suppressed by
      NOT suppressed by
      Other
      Statement
      Reference

      per01, sni1 has short lived phenotype

      (Krishnan et al., 2012)
      Phenotype Manifest In
      Enhanced by
      Statement
      Reference

      sni1 has vacuole | adult stage | progressive phenotype, enhanceable by per01

      (Krishnan et al., 2012)

      sni1 has adult brain | progressive phenotype, enhanceable by per01

      (Krishnan et al., 2012)
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      sni1, per01 double mutants exhibit significant reduction in lifespan compared to single mutants reared in 12h light, 12h dark cycles; exhibit an increase in the neurodegeneration phenotype of sni1 single mutants with increased numbers of and area of vacuoles; and exhibit loss of circadian rhythms similar to that of per01 single mutants. Climbing performance is significantly reduced in sni1, per01 double mutants as compared to sni1 single mutants.

      (Krishnan et al., 2012)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer
      Comments
      Comments

      Precise excision of the P{lacW}sni1 insertion fully rescues the mutant phenotype.

      (Botella et al., 2004)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (1)
      Reported As
      Symbol Synonym
      sni1
      (Rorsman et al., 2025, Krishnan et al., 2012)
      Name Synonyms
      Secondary FlyBase IDs
        References (3)