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.
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.
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.
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.
svspa-pol has visible phenotype, enhanceable by Poxnhs.sev
svspa-pol has increased cell death phenotype, suppressible by BacA\p35GMR.PH
svspa-pol/sv[+] is an enhancer of visible phenotype of EBV\BZLF1GMR.PA
svspa-pol/sv[+] is an enhancer of abnormal size | adult stage phenotype of EBV\BZLF1GMR.PA
svspa-pol/sv[+] is an enhancer of visible phenotype of rgunspecified
svspa-pol is an enhancer of visible phenotype of PoxnUAS.cJa, Scer\GAL4sv.PJ
BacA\p35GMR.PH, svspa-pol has visible phenotype
svspa-pol has lens | somatic clone phenotype, enhanceable by pros[+]/pros17
svspa-pol has cone cell | somatic clone phenotype, enhanceable by pros17
svspa-pol has cone cell phenotype, enhanceable by Poxnhs.sev
svspa-pol has eye phenotype, enhanceable by Poxnhs.sev
svspa-pol has eye disc phenotype, suppressible by BacA\p35GMR.PH
svspa-pol is an enhancer of rhabdomere R7 | increased number phenotype of Scer\GAL4sev.EP, prosL.UAS
svspa-pol/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 is an enhancer of ommatidium phenotype of PoxnUAS.cJa, Scer\GAL4sv.PJ
svspa-pol is a suppressor of cone cell | increased number phenotype of Scer\GAL4sev.EP, prosL.UAS
Scer\GAL4sev.EP, prosL.UAS, svspa-pol has lens phenotype
svspa-pol, ttk1 has ommatidium phenotype
svspa-pol, ttk1 has interommatidial bristle phenotype
svspa-pol, ttk1 has eye photoreceptor cell phenotype
svspa-pol, ttk1 has cone cell | pupal stage phenotype
BacA\p35GMR.PH, svspa-pol has cone cell phenotype
BacA\p35GMR.PH, svspa-pol has secondary pigment cell phenotype
Poxnhs.sev, svspa-pol has lens phenotype
Poxnsv.PJ, svspa-pol has ommatidium phenotype
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.
Strongly enhances the phenotype of wghs.2sev.
The eye phenotype of flies carrying a weakly expressing P{GMR-BZLF1.A} line is enhanced by svspa-pol/+.
Hadorn, Jan. 1951.