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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
Additional Notes
Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype
Nature of the lesion

1.58kb deficiency extending from the second to the fourth intron.

1.58kb deficiency removing exons 3 and 4 and flanking sequences.

1.5kb deficiency deleting two small exons and flanking intron sequences.

Carried on aberration
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

When the majority of eye cells are homozygous svspa-pol mutant using Minute clones, the corneal lenses display slightly irregular shapes and sizes compared with wild-type eyes. The mutant lenses become progressively less defined posteriorly.

Although all cone cells and photoreceptor cells are present in most ommatidia in svspa-pol fly eyes, they display a rough eye resulting from improperly shaped and arranged cone cells.

svspa-pol homozygotes and svrugoso-nu/svspa-pol animals have rough eyes and normal body hairs.

Mutants have cone and pigment cell defects, and photoreceptors are found in the lamina. Mutant eye discs show increased apoptosis compared to controls.

Mutant flies have a rough eye phenotype.

Flies show roughening across the entire eye.

Homozygotes show an almost complete absence of interommatidial bristles. A partial loss or misorientation of ommatidial structures is also seen.

svspa-20/svspa-pol flies have a similar phenotype to svspa-pol flies.

Homozygotes have smaller eyes than normal. The corneal lenses and pseudocones are blurred and irregular. Numerous necrotic pits are seen between an irregular array of ommatidia of variable size. Nearly all bristles in the posterior of the eye have broken or fallen off by the third day after eclosion, although they are initially present when the adults eclose. Most bristles in the anterior of the eye are misplaced or project as doublets from the same vertex. Many ommatidia in adults have the normal number of photoreceptor cells, but show abnormal localisation and orientation of the photoreceptor cells and have malformed rhabdomeres. Other ommatidia have lost between 2 to 5 photoreceptor cells. Many ommatidia appear fused to each other. Cone cells retain their immature round shape and fail to adopt the typical rhomboid-like configuration 24 hours after puparium formation (APF), and some ommatidia lack one of the primary pigment cells. At 45 hours APF most ommatidia are disorganised and their regular lattice is disrupted. The cone cells are abnormal sizes and shapes and fail to form proper contacts with one another, and occasionally one cone cell is lost. Approximately half the ommatidia have lost one or two primary pigment cells, and the remaining primary pigment cell is enlarged and may enclose three of the four cone cells. There are frequently no cells remaining between primary pigment cells of adjacent ommatidia.

svspa-pol/svspa-1 has a more extreme phenotype than svspa-1/svspa-1.

Eyes rather small; surface smooth and glassy. During second day of pupal life, retinula cells withdraw from other cells of eye disk. SEM studies show irregular disposition and morphology of ommatidial hairs as well as numerous necrotic pits over surface of eye (Oster and Crang, 1972); Strum-Tegethoff and Dicke, 1974). ERG absent (Grossfield, 1975). Homozygote has excellent viability and fertility. RK1.

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by

svspa-pol has visible phenotype, enhanceable by Poxnhs.sev

Suppressed by
Enhancer of

svspa-pol, sv[+], sv+ is an enhancer of visible phenotype of EBV\BZLF1GMR.PA

svspa-pol/sv[+] is an enhancer of visible phenotype of rgunspecified

svspa-pol is an enhancer of visible | dominant phenotype of wghs.2sev

Phenotype Manifest In
Enhanced by

svspa-pol has lens | somatic clone phenotype, enhanceable by pros[+]/pros17

svspa-pol has cone cell phenotype, enhanceable by Poxnhs.sev

svspa-pol has eye phenotype, enhanceable by Poxnhs.sev

Suppressed by

svspa-pol has eye disc phenotype, suppressible by BacA\p35GMR.PH

Enhancer of

svspa-pol, sv[+], sv+ is an enhancer of eye phenotype of EBV\BZLF1GMR.PA

svspa-pol/sv[+] is an enhancer of eye phenotype of rgunspecified

svspa-pol is an enhancer of eye phenotype of PoxnUAS.cJa, Scer\GAL4sv.PJ

svspa-pol/sv[+] is an enhancer of phenotype of lzts1

Suppressor of
Additional Comments
Genetic Interactions

pros17 mutants that are also heterozygous for pros17 show a much more severe lens phenotype than either individual mutant, with many ommatidia having reduced, defective, or missing lenses. These mutants also display a reduced number of cone cells per ommatidia.

Lens structures are missing in pros17, svspa-pol double mutants. No cone cells are detected in these mutants.

Overexpression of prosL.Scer\UAS under the control of Scer\GAL4sev.EP in homozygous svspa-pol mutant eyes results in a significant increase in R7 photoreceptor numbers, with three to four often present in individual ommatidia. In addition, no cone cells are detected and adult lenses fail to form.

svspa-pol ttk1 double mutant eyes show a much stronger rough eye phenotype than either single mutant: the surface of the eye is nearly flat with irregularly spaced bristles. Only a few malformed ommatidia, many of which have open holes at their apices, are visible. Photoreceptors in the remaining ommatidia have strongly deformed rhabdomeres. svspa-pol ttk1 pupal eye discs have no cone cells.

The increased cell death seen in svspa-pol eye discs is blocked by BacA\p35GMR.PH, although the adult eye is not rescued in these flies, and it lacks cone cells but has excess secondary pigment cells.

The svspa-pol eye phenotype is enhanced by Poxnhs.sev, with the eye lacking all lenses and most bristles. The number of cone cells present in mid-pupal eye discs is reduced compared to svspa-pol single mutants and those that are seen are smaller than normal and seem to be undergoing apoptosis. Flies carrying two copies of Poxnsv.PJ in a svspa-pol/+ background have a weak rough eye phenotype, which is stronger in a homozygous svspa-pol background.

svspa-pol dominantly enhances the lzts1 phenotype.

Strongly enhances the phenotype of wghs.2sev.

Xenogenetic Interactions

The eye phenotype of flies carrying a weakly expressing P{GMR-BZLF1.A} line is enhanced by svspa-pol/+.

Complementation and Rescue Data
Partially rescued by

svspa-pol is partially rescued by svm11

svspa-pol is partially rescued by svm13

svspa-pol is partially rescued by svm7

svspa-pol is partially rescued by svm10

svspa-pol is partially rescued by svm9

svspa-pol is partially rescued by svm12

svspa-pol is partially rescued by svm14

svspa-pol is partially rescued by svm3

svspa-pol is partially rescued by svhs.PF

Not rescued by

The svspa-pol eye phenotype is partially rescued by expression of svhs.PF using heat shock.

The svspa-pol phenotype is completely rescued by sv+mFa.

Images (1)
Stocks (88)
Notes on Origin

Hadorn, Jan. 1951.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (8)
References (30)