FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Spn27A1
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General Information
Symbol
Dmel\Spn27A1
Species
D. melanogaster
Name
FlyBase ID
FBal0150599
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

Mobilization of P{EP}cupEP2349 caused a 1175bp deletion downstream of the insertion site. This deletion includes the first 275bp of Spn27A.

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

Mutant animals show spontaneous melanisation.

Approximately 6% of homozygotes are viable as adults, and approximately 80% of these escapers show constitutive melanization.

Embryos from Spn27A1 homozygous mothers do not develop beyond the syncytial blastoderm stage. Embryos from Spn27A1/Df(2L)BSC7 mothers show a ventralized phenotype and therefore fail to differentiate a cuticle at the end of embryogenesis. This phenotype can be rescued by injection of Spn27A mRNA.

70% of Spn27A1 mutants die as pupae. Those that survive to adulthood often have wing defects and are female sterile. Ectopic melanisation is seen in mutant adults and larvae in the absence of any injury. Melanization in larvae or adults in response to clean injury, septic injury (with Erwina cartovora) or wasp infection (with L.boulardi), is much more extensive than in similarly treated wild-type animals. In the case of wasp infection or clean injury of larvae, the melanization is usually systemic rather than discrete as in wild-type. 50-70% of mutant larvae pricked with a needle die within 5 hr of injury, compared to 10% of wild-type controls. In most cases, the melanization reaction diffuses throughout the larval body cavity and dead larvae turn completely black. Spn27A1 homozygotes adults have reduced resistance to natural infection with B.bassiana compared to wild-type (survival after 6 days is around 20% compared to around 90% for controls). However, survival 6 days after infection by pricking with cultures of E.coli, M.luteus, or A.fumigata is similar to that after clean injury of mutants.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
Suppressed by
NOT suppressed by
Statement
Reference

Spn27A1 has female sterile phenotype, non-suppressible by PPO1Bc

NOT Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

The spontaneous melanisation seen in Spn27A1 mutant animals is suppressed if they are also mutant for both PPO1Δ and PPO2Δ.

50% of Spn27A1 PPO1Δ double mutant larvae and pupae show a characteristic pattern of melanisation spots under the epidermis.

The spontaneous melanisation seen in Spn27A1 mutant animals is stronger if they are also mutant for PPO2Δ; the double mutant pupae turn black and adults have large spots and wing defects.

The constitutive melanization phenotype of Spn27A1 homozygous escapers is suppressed more than 5-fold if they are also heterozygous for Df(3R)ME15 or Df(3R)dsx11.

The ventralized phenotype that causes the failure of cuticle differentiation in embryos from Spn27A1/Df(2L)BSC7 mothers is abolished when mothers also have the mutant genotype ea4/Df(3R)ea-5022rx1 or spzD1-RPQ/Df(3R)Tl-D. Such embryos have a dorsalized phenotype that is indistinguishable from those produced by single mutant ea4/Df(3R)ea-5022rx1 or spzD1-RPQ/Df(3R)Tl-D mothers.

Pupal lethality, wing phenotypes and ectopic melanisation in larvae after clean injury in Spn27A1 mutants are all suppressed by homozygosity for Bc1. The female sterility phenotype of Spn27A1 mutants is not suppressed.

The melanization response in Bc1 homozygotes is unaffected by Spn27A1, as is the reduced resistance to natural infection with B.bassiana.

Pupal lethality, wing phenotypes and ectopic melanisation in larvae after clean injury in Spn27A1 mutants are all suppressed by homozygosity for Bcunspecified. The female sterility phenotype of Spn27A1 mutants is not suppressed.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Recombinant Spn27A protein purified from S2 cells transfected with Spn27AMtnA.T:SV5\V5,T:Zzzz\His6, rescues ectopic melanisation due to clean injury of Spn27A1 homozygous adults, when injected into the injury site.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
Comments
Comments

Spn27A1 complements cupunspecified : Unlike Spn27A1 or cupunspecified homozygotes, Spn27A1/cupunspecified females are not sterile.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (8)