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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
spn-A057, spnA057, Rad51057
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
Additional Notes
Nucleotide change:


Amino acid change:

A205V | spn-A-PA; A148V | spn-A-PB

Reported amino acid change:



Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype
Nature of the lesion

Amino acid replacement: A205V.

Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 0 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Disease-implicated variant(s)
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description

Larval exposure to hydroxyurea does not affect spn-A3/spn-A3 adult survival rates.

Mutants show sensitivity to ionising radiation compared to controls, with almost no survival of the mutants after exposure to 750rads ionising radiation.

spn-A3/spn-A093A males in which excision of an insertion of P{hswa} is induced during development are completely viable.

spn-A3/spn-A093A third instar larvae show increased sensitivity to high doses of gamma irradiation compared to controls.

The complete copia element in wa.hs has an LTR at each end. Following excision of P{hswa}, repair by SDSA (synthesis-dependent strand annealing) can lead to excision of this copia element due to annealing at these LTRs, resulting in red eyed progeny. Incomplete SDSA, where joining has occurred independently of annealing of homologous ends, can delete parts of the w ORF in wa.hs resulting in yellow eyed progeny. The frequency of red eyed progeny (and therefore of complete SDSA) following excision of P{hswa}sdwa using H{PΔ2-3}HoP2.1 is decreased from 6% to zero in a spn-A3/spn-A093A background, but the frequency of yellow eyed progeny (and therefore of incomplete SDSA) is increased from 10% to 17%. This background does not significantly affect the proportion of hemizygous lethal sd deletions resulting from this excision, but does decrease the proportion of excisions resulting non-lethal deletions (from 7% to 1.7%).

In contrast to wild-type ovaries, where the synaptonemal complex (SC) is always restricted to the oocyte by region 2b, spn-A3 mutant females show a significant delay in the process, with cysts with more than 1 cell in synapsis in region 3 of the germarium and in stage 1 and stage 2 of the vitellarium.

Transheterozygous eggs with spn-A2 exhibit either a strong or weak ventralised phenotype: eggs are longer than wild type and are completely symmetric along the DV axis or the eggs display fused dorsal appendages. Germline clones in egg chambers are composed of wild type follicle cells, mutant nurse cells, misplaced oocyte, oocytes that give rise to ventralised eggs and oocytes that lack a karyosome.

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Suppressed by
NOT suppressed by
Enhancer of

spn-A3/spn-A3 is an enhancer of short lived | chemical conditional phenotype of WRNexoΔ

NOT Enhancer of
NOT Suppressor of
Phenotype Manifest In
Enhanced by

spn-A3 has phenotype, enhanceable by spn-D2

Suppressed by

spn-A093A/spn-A3 has egg chorion phenotype, suppressible by eIF1ABH167/eIF-1A[+]

Enhancer of

spn-A3 is an enhancer of phenotype of spn-D2

spn-A3 is an enhancer of oocyte phenotype of spn-D2

Additional Comments
Genetic Interactions

The hypersensitivity of Df(3R)mus308Δ/Df(3R)mus308Δ;spn-A3/spn-A093A double mutant third instar larvae to ionizing radiation is rescued by combination with either the mus308+tBa or the mus308ATPase-dead transgene but not by mus308pol-dead.

Df(3R)mus308Δ/Df(3R)mus308Δ;spn-A3/spn-A093A mutants show a significant reduction in the frequency of end joining repair events in a P{hsw[a]}-excision repair assay, which can be rescued with mus308+tBa and mus308ATPase-dead but not mus308pol-dead.

spn-A3/spn-A3 enhances hydroxyurea sensitivity (decreases adult survival) in WRNexoΔ/WRNexoΔ mutants.

eIF-1ABH167 dominantly suppresses the eggshell patterning defects in spn-A3/spn-A093A mutants.

spn-A3 mus308D5 double mutant animals are extremely sensitive to ionising radiation, with almost no survival of the mutants after exposure to 125rads ionising radiation.

There is a decrease in the percentage of end-joining repair products in studies of excision and repair events of P{hswa} in spn-A3 mus308D2/spn-A3 mus308ZIII-2003, spn-A3 mus308D2/spn-A3 mus308D2 and spn-A093A mus308D5/spn-A3 mus308ZIII-2003 double mutant males compared to the percentage seen in spn-A single mutants. The double mutants show a substantial increase in the percentage of deletion-associated repair events isolated compared to controls, as occurs in mus308 single mutants. These males show increased sterility.

spn-A3 mus308D2/spn-A3 mus308ZIII-2003 double mutant males in which excision of P{hswa} is occurring show morphological defects such as abdominal cuticle mispatterning.

The spn-A3/spn-A093A transheterozygous condition does not suppress the lethality of mus312D1/mus312Z1973, mus309D2/mus309N1 double mutants.

The lethality seen in mei-4129D males in which excision of an insertion of P{hswa} is induced during development is completely suppressed by spn-A3/spn-A093A.

At intermediate doses (400-500 rad) of gamma irradiation, Lig4169 spn-A3/spn-A093A double mutant larvae show increased sensitivity to irradiation compared to spn-A3/spn-A093A single mutants.

spn-A3/spn-A093A suppresses the increase deletions resulting from the H{PΔ2-3}HoP2.1 driven of excision of P{hswa}sdwa due to a mus309D2/mus309D3 background.

The phenotype of a delay in the restriction of the synaptonemal complex seen in the female germline of spn-D2 or spn-A3 single mutants is enhanced in spn-D2 spn-A1 double mutants.

Double mutant stage 5-6 egg chambers with mus301094, spn-D2 or spn-E1 exhibit a two-oocyte phenotype: the second pro-oocyte develops as an oocyte rather than a nurse cell. The double mutants delay but do not block the decision between the two pro-oocytes as one of the two cells always becomes a nurse cell eventually.

Xenogenetic Interactions
Complementation and Rescue Data
Images (0)
Stocks (0)
Notes on Origin

Strong mutation.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (9)
References (22)