FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\spg2
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General Information
Symbol
Dmel\spg2
Species
D. melanogaster
Name
FlyBase ID
FBal0015995
Feature type
allele
Associated gene
Dmel\spg
Associated Insertion(s)
Carried in Construct
Also Known As
spg242
Key Links
Genomic Maps

Allele class
Mutagen
Nature of the Allele
Allele class
Mutagen
ethyl methanesulfonate
(Postner et al., 1992, Tearle and Nusslein-Volhard, 1987)
Progenitor genotype
Cytology
Description

Amino acid replacement: W487term.

(Biersmith et al., 2011)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
point_mutation
3R:28,863,840..28,863,840 [+]
Nucleotide change:

G28863840A

Amino acid change:

W457term | spg-PD; W457term | spg-PE; W457term | spg-PF; W457term | spg-PG; W457term | spg-PH

Reported amino acid change:

W487term

Comment:

The difference between the reported and annotated locations of the spg2 mutation are based on updates to the structure of the spg transcripts that predict 30 fewer amino acids in the amino terminal part of the spg protein compared to r5.1. G to A nucleotide change at the second or third position of the Trp codon leads to a nonsense mutation (exact site of mutation unspecified). Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

(Biersmith et al., 2011)
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 ( 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

      Eggs produced from spg2 homozygous mothers with a mutant paternal spg2 allele die early in embryonic development.

      Homozygous spg2 or spg2/Df(3R)3450 or spg2/spg3 embryos exhibit minor defects in axonal patterns: infrequent breaks in the outer longitudinal tract and occasional thinning of these tracts.

      Homozygous spg2 embryos do not exhibit myoblast fusion defects.

      (Biersmith et al., 2011)

      Embryos from homozygous mutant spg females lack actin caps over interphase nuclei at the syncytial blastoderm stage. Embryos from mothers carrying combinations of spg1, spg2 or spg335 die soon after gastrulation.

      (Postner et al., 1992)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Phenotype Manifest In
      Enhanced by
      Statement
      Reference

      spg2 has lateral longitudinal fascicle phenotype, enhanceable by Ced-1219F3

      (Biersmith et al., 2011)
      NOT Enhancer of
      Statement
      Reference

      spg2 is a non-enhancer of embryonic myoblast phenotype of mbcD11.2

      (Biersmith et al., 2011)

      spg2 is a non-enhancer of lateral longitudinal fascicle phenotype of mbcD11.2

      (Biersmith et al., 2011)
      Other
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      Compared to Ced-1219F3/Ced-1219F3 or spg2/spg2 single mutants, a consistent increase in longitudinal axon defects is observed in the double homozygous mutants. There is also an increase in axons that inappropriately cross the midline, and abnormalities in the spacing between adjacent segments is enhanced.

      The final muscle pattern in Ced-1219F3/Ced-1219F3, spg2/spg2 double mutant embryos appears wild type.

      In mbcD11.2/mbcD11.2, spg2/spg2 double mutants, myoblasts fail to fuse but still cluster around the founder cells (as in mbcD11.2/mbcD11.2 mutants).

      There is no significant increase in broken fascicles or the collapse of the outer longitudinal tracts in mbcD11.2, spg2 double mutants over mbcD11.2 mutants alone. However, there is an increase in midline fascicle crossing in the double mutants. Abnormal positioning of the ventral nerve cord is also observed in the double mutants.

      Df(2L)CadNΔ14/+ in a spg2 homozygous background increases the occurrence of axon outgrowth defects over those seen in spg2 alone. Df(2L)CadNΔ14/Df(2L)CadNΔ14, spg2 embryos show more severe defects, with greater than additive increase in ectopic midline crossing.

      (Biersmith et al., 2011)

      mbcD11.2 spg2 double mutant embryos have a roughly comparable overall level of myoblast fusion compared to mbcD11.2 single mutant embryos.

      (Haralalka et al., 2011)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Rescued by

      spg2 is rescued by Scer\GAL4nanos.PG/spgUAS.cBa

      (Biersmith et al., 2011)
      Comments

      The early lethality associated with embryos produced from spg2 homozygous mothers with a mutant paternal spg2 allele is rescued by expressing spgScer\UAS.cBa with Scer\GAL4nos.PG.

      (Biersmith et al., 2011)
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (3)
      Reported As
      Symbol Synonym
      spg242
      (Biersmith et al., 2011, Haralalka et al., 2011, Pichler et al., 2003, Postner et al., 1992, Tearle and Nusslein-Volhard, 1987)
      spg2
      sponge242
      (Schmidt et al., 2018)
      Name Synonyms
      Secondary FlyBase IDs
        References (6)