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

Deletion from 3983 to 5181bp in the last intron.

1.3kb deletion in the terminal intron of the so gene.

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

glial cell & larval optic lobe

lamina & neuron

Detailed Description

so1 mutant larval eye discs display increased level of cell death (detected by antibody staining) during development.

so1 mutants exhibit normal light-dependent temperature preference. Similarly to wild-type, they prefer higher temperature in the light than in the dark.

Mutants completely lack compound eyes.

Eye disc size in so1 mutant clones is similar to wild type.

so1 mutants lack eyes.

The optic stalk grows normally in mutant animals (although it fails to maintain a round-shaped cross section), despite a complete lack of photoreceptor cells.

so1 mutants completely lack compound eyes.

so1 mutants have a small eye disc and show a complete loss of the retina.

so1 mutant clones in the eye over-proliferate and either die or, if they survive, develop cuticle in the adult eye. so1 larvae have small eye discs and adults are either eyeless or have very small eyes.

Lamina glial cell migration occurs in so1 mutants to some extent, although these glial cells fail to form the normal three-layer structures.

In the optic lobes of so1 mutant larvae, photoreceptor axon innervation is partially or completely absent. In regions where innervation has failed, glial cell migration fails. These glial cells accumulate at the point where they would have joined axon fascicles on paths towards neuropil destinations. This results in varying degrees of loss of inner chiasm and medulla neuropil glial cell layers. By late third instar, the medulla neuropil is somewhat disorganized in these animals, and there is a significant increase in the number of apoptotic cells throughout the medulla cortex. These apoptotic cells are concentrated in regions where glial cells have been lost, and in the area next to the deformed neuropil.

The region normally occupied by the eyes is replaced by surrounding head tissue in so1 adults.

so1 mutants can completely lack compound eyes, although this phenotype is not fully penetrant; in mutants that are eyeless, the optic lobes are aberrantly small. so1 flies lack the ocelli, but always have an intact eyelet. The ability of so1 flies to e-entrain to 6 hour phase advances of the LD cycle is different to wild type as mutants need several days to re-entrain and show extended activity into the dark phase. so1 flies fail to entrain to wavelengths longer than 550nm, while wild-type flies show sensitivity into the red part of the spectrum. Some so1 flies fail to entrain to green light after the second phase advance and only show a morning peak of activity during the blue LD cycle after the first phase shift. Many so1 flies show antidromic phase shifting, where the clock delays its phase by 18 hours instead of advancing its phase by 6 hours, in green light. Wild-type flies show a morning and evening activity peak at high and intermediate irradiances, but can lack the morning peak at low irradiances. In contrast, only half of so1 flies show two peaks at high irradiances and only a quarter show two peaks at intermediate irradiances. At low irradiances, all so1 flies show only the morning peak. The phase relationship of the evening peak is dependent on wavelength in so1 flies, while no such dependency is seen in wild type.

Homozygous mutant larvae exhibit an early onset glial cell migration defect in the developing eye.

The optic lobes are much reduced in mutant pupae and lack a lamina.

Mutants lack both the compound eyes and ocelli.

Only a few ommatidia form in the eye disc. Lamina development is restricted to the immediate vicinity of the small number of axons that grow into the lamina target field.

Homozygous clones in the eye disc show massive overgrowth followed by cell death. Propagation of the morphogenetic furrow does not occur in homozygous clones in the eye disc. Less than 5% of homozygous eye discs show development of the neuronal array. More than 95% of adult homozygotes are completely eyeless.

The eyes are absent in homozygotes, but they are not replaced by frons cuticle.

Third instar foraging larvae show negative photobehaviour indistinguishable from the wild-type response to light. Third instar larvae show a decrease in negative phototaxis from the onset of wandering culminating in random photobehaviour indistinguishable from the response of wild-type larvae.

Homozygotes lack compound eyes and ocelli. so1/so3 flies have widely varying eye defects ranging from completely normal eyes bilaterally to flies whose eyes have been partially replaced with bilateral cuticular protrusions of non-eye tissue. Homozygous eye discs display massive cell death anterior to the morphogenetic furrow. The optic lobe primordium of homozygotes is reduced in size and movement into the head cavity is arrested at an early stage so it fails to invaginate.

Migration of the retinal basal glia from the optic stalk to the eye disc does not occur.

Heterozygotes with somda are wild type. Homozygotes display a small eye.

Homozygotes lack eyes and ocelli or are reduced. Reduced viability at high temperatures.

The arborisation field of the pigment-dispersing hormone-immunoreactive neurons in the medulla is smaller than in wild-type flies. Immunoreactive fibres sometimes leave the posterior optic tract and project to the dorsal protocerebrum towards the calyces of the mushroom bodies.

Ommatidia develop in reduced numbers or are entirely absent. Ommatidia develop within a single area that can be found in different position in different discs. Retinal axons develop to the appropriate area of the developing lamina. Retinal axon fascicles must be capable of proper navigation in the absence of a full complement of neighbouring axons.

Ocelli always absent; eyes usually reduced to small groups of ommatidia and occasionally missing; eye

field sometimes in form of an eye stalk protruding

from head with an irregular arrangement of ommatidia;

heavy ommatidial disruption with many receptor cells

missing. Optic lobes reduced in size and many flies

have no lamina. The reduced volume of adult optic

lobes is due to accentuated degeneration of precursor

neurons that occurs to a certain degree in normal

pupal development (Fischbach, 1983); the increased

severity in the mutant includes degeneration of axons

in second optic chiasma (Fischbach and Technau, 1984);

sol enhances this kind of degeneration, but acts on a

separate set of precursors for columnar visual system

neurons--as confirmed by anatomical analysis of sol;

so double mutant, which ends up with tiny, rudimentary

optic lobes (Fischbach and Technau, 1984); sol; so

also leads to a central brain that is smaller than

normal due to missing afferents from visual system

(Fischbach and Technau, 1984); more specifically,

there is a reduction in number of axons in anterior

optic track in so and combining so with sol causes a

further reduction, but again, these two genes act

independently on separate subsets of such axons

(Fischbach and Lyly-Hunerberg, 1983). Histological

studies reveal that the eye-antenna disc in third

instar larvae appears normal until differentiation

begins, at which time cell death is observed (Hofbauer

and Campos-Ortega). More extreme at elevated

temperatures; reduced-viability at 30oC;

temperature-sensitive period for eye defect in third

instar. Survival sensitive to elevated temperature at

all developmental stages (Ransom, 1980). Mosaic

studies demonstrate that so acts in developing eye

tissue and that the resulting reduction in retinal

innervation leads to death of cells in the lamina and

breakdown of medulla and lobula-complex neuropil

(Fischback and Technau). Nonphototactic (Benzer, 1967)

and visual orientation almost absent (Bulthoff, 1982).

Studies of circadian rhythms in so show eclosion to be

normally periodic (Engelmann and Honneger, 1966);

adult activity rhythms are robust, in that so, even

when thoroughly eyeless, responds to light:dark cues

such that it entrains to these conditions (is

periodically active vs. inactive and anticipates the

environmental transitions) and subsequently free-runs

with obvious circadian periodicities in constant

darkness (Helfrich and Engelmann, 1983; Dushay,

Rosbash, and Hall, 1989); however, these behavioral

rhythms are frequently aberrant, e.g., with 'split'

active components appearing after several days of

free-run and with dual periodicities extractable from

the locomotor data (Helfrich, 1986); nearly all adults

are dual-period when so combined with sol (Helfrich, 1986).

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Enhancer of
Phenotype Manifest In
Enhanced by

so1 has eye phenotype, enhanceable by gl60j

so1 has photoreceptor cell phenotype, enhanceable by gish1

Suppressed by
NOT suppressed by

so1 has eye phenotype, non-suppressible by Mmus\Six3UAS.cWa/Scer\GAL4ey.PU

so1 has eye phenotype, non-suppressible by Mmus\Six5UAS.cWa/Scer\GAL4ey.PU

so1 has eye phenotype, non-suppressible by Mmus\Six6UAS.cWa/Scer\GAL4ey.PU

so1 has eye phenotype, non-suppressible by so::OptixSD.UAS/Scer\GAL4ey.PU

so1 has eye phenotype, non-suppressible by so::OptixCT.UAS/Scer\GAL4ey.PU

so1 has eye phenotype, non-suppressible by so::OptixNT+CT.UAS/Scer\GAL4ey.PU

so1 has eye phenotype, non-suppressible by so::OptixSD+HD.UAS/Scer\GAL4ey.PU

Enhancer of
NOT Enhancer of

so1 is a non-enhancer of eye phenotype of pbRev3.HSPB

Additional Comments
Genetic Interactions

Scer\GAL4ey.PU-mediated expression of Six4Scer\UAS.cCa significantly rescues the so1 eye phenotype.

gl60j; so1 double mutants are completely eyeless and the eyelet is absent. These double mutants can only re-entrain to wavelengths shorter than 450nm, while so1 single mutants can entrain to wavelengths up to 550nm. Unlike so1 single mutants, phase relationship the evening peak activity of gl60j; so1 double mutants is not dependent on wavelength and these flies rarely show antidromic phase shifting. so1; cryb double mutants have the same partially penetrant eye phenotype as so1 single mutants. When these mutants have eye remnants, they can re-entrain to to 6 hour phase advances of the LD cycle in green or red light, but not blue light. When these mutants are completely eyeless, they are unable to re-entrain at any wavelength and their evening activity peak occurs after lights off, while flies with eye remnants show a peak of activity two hours before lights off, as do wild-type flies. Unlike so1 single mutants, so1; cryb double mutants rarely show antidromic phase shifting.

Expression of eyScer\UAS.cHa using Scer\GAL4dpp.blk1 in a so1/so1 background does not lead to the formation of ectopic eyes. Expression of toyScer\UAS.cCa using Scer\GAL4dpp.blk1 in a so1/so1 background leads to the formation of ectopic eyes.

When eyScer\UAS.cHa is driven by Scer\GAL4dpp.blk1 in a so1 or eya1 background, no eye structures appear but legs are reduced/deformed. When eyScer\UAS.cHa expression is driven by Scer\GAL4dpp.blk1 in a so1 background ectopic cell death occurs in the region of the wing disc that would lead to extra eyes in a wild type background.

Xenogenetic Interactions

Scer\GAL4ey.PU-mediated expression of Mmus\Six1Scer\UAS.cWa or Mmus\Six2Scer\UAS.cWa significantly rescues, while expression of Mmus\Six4Scer\UAS.cWa weakly rescues the so1 eye phenotype.

Complementation and Rescue Data

Expression of soScer\UAS.FL.NT.T:Hsim\VP16 under the control of Scer\GAL4ey.PU restores eye development almost to wild type in so1 flies.

Expression of soScer\UAS.FL.CT.T:Hsim\VP16 under the control of Scer\GAL4ey.PU partially restores eye development in so1 flies.

Expression of soScer\UAS.FL.NT.T:Rep-en under the control of Scer\GAL4ey.PU fails to restore eye development in so1 flies.

Expression of soso11-soAE rescues the eyeless and partially rescues the ocelliless phenotypes of so1.

Scer\GAL4ey.PU-mediated expression of soFL.Scer\UAS, soΔNT.Scer\UAS, soΔCT.Scer\UAS or soΔNT+CT.Scer\UAS restores so1 eyes to near wild type.

Scer\GAL4ey.PU-mediated expression of soΔSD.Scer\UAS or soΔHD.Scer\UAS does not rescue the so1 eye phenotype.

soso10-soAE.hs rescues ocellus and eye development in so1 mutant flies. The lateral ocelli appear almost normal, while the size of the anterior ocellus is reduced.

Expression of soScer\UAS.cPa under the control of Scer\GAL4so.10 or Scer\GAL4so.10.TOYmt rescues the missing eyes of so1 animals, but not the ocelli. Expression of soScer\UAS.cPa under the control of Scer\GAL4so.10.EY.TOYmt.1.2.5 only partially rescues the missing eyes of so1 animals; almost 100% of the flies have a strongly reduced eye on one side of the head and no eye on the other side. Expression of soScer\UAS.cPa under the control of Scer\GAL4so.7 fully rescues the missing eyes of so1 animals, and partially rescues the ocelli. Expression of soScer\UAS.cPa under the control of Scer\GAL4so.7.EY.TOYmt.1.2.5 does not rescue the missing eyes of so1 animals but rescues the ocelli. Expression of soScer\UAS.cPa under the control of Scer\GAL4so.7.TOYmt rescues the missing eyes of so1 animals but does not rescue the ocelli. Expression of soScer\UAS.cPa under the control of Scer\GAL4so.7.EY+TOYmt.1-5 does not rescue the missing eyes or ocelli of so1 animals.

The neuronal array phenotype in the eye disc is rescued along the posterior and lateral but not the anterior portions of the disc by soScer\UAS.cPa expressed under the control of Scer\GAL4dpp.blk1 (the region of rescue correlates well with the domain of Scer\GAL4dpp.blk1 expression). More than 95% of adult homozygotes are completely eyeless. The most posterior region of the adult eye is rescued by soScer\UAS.cPa expressed under the control of Scer\GAL4E132.

Heat-induced so expression completely rescues the eyeless phenotype (a single short heat pulse delivered in late second or early third instar).

Images (1)
Stocks (2)
Notes on Origin

Milani, 1939.


No interaction with P{sev-svp1} or P{sev-svp2} exists.

Mutant phenotype can be rescue by introduction of P{hsp70/so} and heat pulses during eye-antennal imaginal disc development.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (59)