FlyBase Allele Report: Dmel\so[1]

General Information

Symbol

Dmel\so¹

Species

D. melanogaster

Name

FlyBase ID

FBal0015924

Feature type

allele

Associated gene

Dmel\so

Associated Insertion(s)

Carried in Construct

Key Links

Allele class

loss of function allele

Mutagen

spontaneous

Nature of the Allele

Allele class

loss of function allele

(Pignoni et al., 1997)

Mutagen

spontaneous

(Cheyette et al., 1994, Heitzler et al., 1993)

Progenitor genotype

Cytology

Description

Deletion from 3983 to 5181bp in the last intron.

(Kenyon et al., 2005)

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

(Cheyette et al., 1994)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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

adult optic lobe

(Helfrich-Forster et al., 2002, Malpel et al., 2002)

adult subretinal glial cell

(Hummel et al., 2002, Choi and Benzer, 1994)

Bolwig organ

(Cheyette et al., 1994)

cell body rind of adult medulla

(Dearborn and Kunes, 2004)

cuticle | ectopic | somatic clone

(Kenyon et al., 2005)

embryonic/larval optic stalk

(Murakami et al., 2007)

eye

(Head et al., 2015, Anderson et al., 2012, Weasner and Kumar, 2009, Weasner et al., 2007, Kumar et al., 2004, Helfrich-Forster et al., 2002, Punzo et al., 2002, Pignoni et al., 1997, Royet and Finkelstein, 1997, Cheyette et al., 1994, Choi and Benzer, 1994, Serikaku and O'Tousa, 1994, Heitzler et al., 1993)

eye | somatic clone

(Kenyon et al., 2005)

eye disc

(Anderson et al., 2006, Huang et al., 1998, Pignoni et al., 1997)

eye disc | somatic clone

(Kenyon et al., 2005, Pignoni et al., 1997)

eye disc | third instar larval stage

(Weasner et al., 2016)

eye disc morphogenetic furrow | somatic clone

(Pignoni et al., 1997)

eye photoreceptor cell

(Murakami et al., 2007)

glial cell & larval optic lobe

(Dearborn and Kunes, 2004)

lamina

(Yoshida et al., 2005, Malpel et al., 2002)

lamina & neuron

(Huang et al., 1998)

lamina anlage glial cell

(Yoshida et al., 2005, Hummel et al., 2002)

medulla anlage

(Dearborn and Kunes, 2004)

ocellus

(Head et al., 2015, Helfrich-Forster et al., 2002, Punzo et al., 2002, Cheyette et al., 1994, Choi and Benzer, 1994, Heitzler et al., 1993)

ommatidium

(Huang et al., 1998, Kunes et al., 1993)

Pdf neuron

(Helfrich-Forster and Homberg, 1993)

retina

(Anderson et al., 2006)

visual primordium

(Cheyette et al., 1994)

Detailed Description

Statement

Reference

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

(Weasner et al., 2016)

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

(Head et al., 2015)

Mutants completely lack compound eyes.

(Anderson et al., 2012)

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

(Wang and Sun, 2012)

so¹ mutants lack eyes.

(Weasner and Kumar, 2009)

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.

(Murakami et al., 2007)

so¹ mutants completely lack compound eyes.

(Weasner et al., 2007)

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

(Anderson et al., 2006)

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.

(Kenyon et al., 2005)

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

(Yoshida et al., 2005)

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.

(Dearborn and Kunes, 2004)

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

(Kumar et al., 2004)

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.

(Helfrich-Forster et al., 2002)

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

(Hummel et al., 2002)

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

(Malpel et al., 2002)

Mutants lack both the compound eyes and ocelli.

(Punzo et al., 2002)

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.

(Huang et al., 1998)

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.

(Pignoni et al., 1997)

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

(Royet and Finkelstein, 1997)

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.

(Sawin-McCormack et al., 1995)

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.

(Cheyette et al., 1994)

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

(Choi and Benzer, 1994)

Heterozygotes with so^mda are wild type. Homozygotes display a small eye.

(Serikaku and O'Tousa, 1994)

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

(Heitzler et al., 1993)

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.

(Helfrich-Forster and Homberg, 1993)

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.

(Kunes et al., 1993)

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 30^oC;

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

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

so¹ has abnormal circadian rhythm phenotype, enhanceable by cry^b

(Helfrich-Forster et al., 2002)

so¹ has abnormal circadian rhythm phenotype, enhanceable by gl^60j

(Helfrich-Forster et al., 2002)

Enhancer of

Statement

Reference

so¹ is an enhancer of visible phenotype of H^UAS.cMa, Scer\GAL4^GMR.PF

(Müller et al., 2005)

Other

Statement

Reference

Scer\GAL4^dpp.blk1, so¹, toy^UAS.cCa has visible phenotype

(Niimi et al., 1999)

Phenotype Manifest In

Enhanced by

Statement

Reference

so¹ has eye phenotype, enhanceable by gl^60j

(Helfrich-Forster et al., 2002)

so¹ has photoreceptor neuron phenotype, enhanceable by gish¹

(Hummel et al., 2002)

Suppressed by

Statement

Reference

so¹ has eye phenotype, suppressible by Six4^UAS.cCa/Scer\GAL4^ey.PU

(Weasner and Kumar, 2009)

so¹ has eye phenotype, suppressible by Mmus\Six1^UAS.cWa/Scer\GAL4^ey.PU

(Weasner and Kumar, 2009)

so¹ has eye phenotype, suppressible by Mmus\Six2^UAS.cWa/Scer\GAL4^ey.PU

(Weasner and Kumar, 2009)

so¹ has eye phenotype, suppressible by Mmus\Six4^UAS.cWa/Scer\GAL4^ey.PU

(Weasner and Kumar, 2009)

so¹ has eye phenotype, suppressible by so::Optix^NT.UAS/Scer\GAL4^ey.PU

(Weasner et al., 2007)

so¹ has eye phenotype, suppressible by so::Optix^HD.UAS/Scer\GAL4^ey.PU

(Weasner et al., 2007)

NOT suppressed by

Statement

Reference

so¹ has eye phenotype, non-suppressible by Mmus\Six3^UAS.cWa/Scer\GAL4^ey.PU

(Weasner and Kumar, 2009)

so¹ has eye phenotype, non-suppressible by Mmus\Six5^UAS.cWa/Scer\GAL4^ey.PU

(Weasner and Kumar, 2009)

so¹ has eye phenotype, non-suppressible by Mmus\Six6^UAS.cWa/Scer\GAL4^ey.PU

(Weasner and Kumar, 2009)

so¹ has eye phenotype, non-suppressible by Optix^FL.UAS/Scer\GAL4^ey.PU

(Weasner and Kumar, 2009, Weasner et al., 2007)

so¹ has eye phenotype, non-suppressible by so::Optix^SD.UAS/Scer\GAL4^ey.PU

(Weasner et al., 2007)

so¹ has eye phenotype, non-suppressible by so::Optix^CT.UAS/Scer\GAL4^ey.PU

(Weasner et al., 2007)

so¹ has eye phenotype, non-suppressible by so::Optix^NT+CT.UAS/Scer\GAL4^ey.PU

(Weasner et al., 2007)

so¹ has eye phenotype, non-suppressible by so::Optix^SD+HD.UAS/Scer\GAL4^ey.PU

(Weasner et al., 2007)

Enhancer of

Statement

Reference

so¹ is an enhancer of eye phenotype of H^UAS.cMa, Scer\GAL4^GMR.PF

(Müller et al., 2005)

so¹ is an enhancer of photoreceptor neuron phenotype of gish¹

(Hummel et al., 2002)

NOT Enhancer of

Statement

Reference

so¹ is a non-enhancer of eye phenotype of pb^Rev3.HSPB

(Benassayag et al., 2003)

Other

Statement

Reference

Scer\GAL4^dpp.blk1, so¹, toy^UAS.cCa has eye | ectopic phenotype

(Niimi et al., 1999)

Scer\GAL4^dpp.blk1, ey^UAS.cHa, so¹ has leg phenotype

(Halder et al., 1998)

Scer\GAL4^dpp.blk1, ey^UAS.cHa, so¹ has wing disc phenotype

(Halder et al., 1998)

Additional Comments

Genetic Interactions

Statement

Reference

Scer\GAL4^ey.PU-mediated expression of Six4^Scer\UAS.cCa significantly rescues the so¹ eye phenotype.

(Weasner and Kumar, 2009)

gl^60j; 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 gl^60j; so¹ double mutants is not dependent on wavelength and these flies rarely show antidromic phase shifting. so¹; cry^b 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; cry^b double mutants rarely show antidromic phase shifting.

(Helfrich-Forster et al., 2002)

Expression of ey^Scer\UAS.cHa using Scer\GAL4^dpp.blk1 in a so¹/so¹ background does not lead to the formation of ectopic eyes. Expression of toy^Scer\UAS.cCa using Scer\GAL4^dpp.blk1 in a so¹/so¹ background leads to the formation of ectopic eyes.

(Niimi et al., 1999)

When ey^Scer\UAS.cHa is driven by Scer\GAL4^dpp.blk1 in a so¹ or eya¹ background, no eye structures appear but legs are reduced/deformed. When ey^Scer\UAS.cHa expression is driven by Scer\GAL4^dpp.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.

(Halder et al., 1998)

Xenogenetic Interactions

Statement

Reference

Scer\GAL4^ey.PU-mediated expression of Mmus\Six1^Scer\UAS.cWa or Mmus\Six2^Scer\UAS.cWa significantly rescues, while expression of Mmus\Six4^Scer\UAS.cWa weakly rescues the so¹ eye phenotype.

(Weasner and Kumar, 2009)

Complementation and Rescue Data

Rescued by

so¹ is rescued by so^{VP16.UAS.FL.NT}/Scer\GAL4^ey.PU

(Anderson et al., 2012)

so¹ is rescued by so^FL.UAS/Scer\GAL4^ey.PU

(Weasner et al., 2007)

so¹ is rescued by so^ΔNT.UAS/Scer\GAL4^ey.PU

(Weasner et al., 2007)

so¹ is rescued by so^ΔCT.UAS/Scer\GAL4^ey.PU

(Weasner et al., 2007)

so¹ is rescued by so^ΔNT+CT.UAS/Scer\GAL4^ey.PU

(Weasner et al., 2007)

so¹ is rescued by so^UAS.cPa/Scer\GAL4^hs.PB

(Kenyon et al., 2005)

so¹ is rescued by so^G66A.hs

(Kenyon et al., 2005)

so¹ is rescued by so^so10-soAE.hs

(Pauli et al., 2005)

so¹ is rescued by so^hs.PC

(Cheyette et al., 1994)

Partially rescued by

so¹ is partially rescued by so^{VP16.UAS.FL.CT}/Scer\GAL4^ey.PU

(Anderson et al., 2012)

so¹ is partially rescued by so^so11-soAE

(Blanco et al., 2010)

so¹ is partially rescued by so^UAS.cPa/Scer\GAL4^{so.10.EY.TOYmt.1.2.5}

(Punzo et al., 2002)

so¹ is partially rescued by so^UAS.cPa/Scer\GAL4^so.10.TOYmt

(Punzo et al., 2002)

so¹ is partially rescued by so^UAS.cPa/Scer\GAL4^{so.7.EY.TOYmt.1.2.5}

(Punzo et al., 2002)

so¹ is partially rescued by so^UAS.cPa/Scer\GAL4^so.7.TOYmt

(Punzo et al., 2002)

so¹ is partially rescued by so^UAS.cPa/Scer\GAL4^so.7

(Punzo et al., 2002)

so¹ is partially rescued by so^UAS.cPa/Scer\GAL4^so.10

(Punzo et al., 2002)

so¹ is partially rescued by so^UAS.cPa/Scer\GAL4^upd1-E132

(Pignoni et al., 1997)

so¹ is partially rescued by so^UAS.cPa/Scer\GAL4^dpp.blk1

(Pignoni et al., 1997)

Not rescued by

so¹ is not rescued by so^{UAS.FL.NT.EnR}/Scer\GAL4^ey.PU

(Anderson et al., 2012)

so¹ is not rescued by so^ΔSD.UAS/Scer\GAL4^ey.PU

(Weasner et al., 2007)

so¹ is not rescued by so^ΔHD.UAS/Scer\GAL4^ey.PU

(Weasner et al., 2007)

so¹ is not rescued by so^L257P.UAS/Scer\GAL4^hs.PB

(Kenyon et al., 2005)

so¹ is not rescued by so^UAS.cPa/Scer\GAL4^{so.10.EY+TOYmt.1-5}

(Punzo et al., 2002)

so¹ is not rescued by so^UAS.cPa/Scer\GAL4^{so.7.EY+TOYmt.1-5}

(Punzo et al., 2002)

Comments

Expression of so^{Scer\UAS.FL.NT.T:Hsim\VP16} under the control of Scer\GAL4^ey.PU restores eye development almost to wild type in so¹ flies.

Expression of so^{Scer\UAS.FL.CT.T:Hsim\VP16} under the control of Scer\GAL4^ey.PU partially restores eye development in so¹ flies.

Expression of so^{Scer\UAS.FL.NT.T:Rep-en} under the control of Scer\GAL4^ey.PU fails to restore eye development in so¹ flies.

(Anderson et al., 2012)

Expression of so^so11-soAE rescues the eyeless and partially rescues the ocelliless phenotypes of so¹.

(Blanco et al., 2010)

Scer\GAL4^ey.PU-mediated expression of so^FL.Scer\UAS, so^{ΔNT.Scer\UAS}, so^{ΔCT.Scer\UAS} or so^{ΔNT+CT.Scer\UAS} restores so¹ eyes to near wild type.

Scer\GAL4^ey.PU-mediated expression of so^{ΔSD.Scer\UAS} or so^{ΔHD.Scer\UAS} does not rescue the so¹ eye phenotype.

(Weasner et al., 2007)

so^so10-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.

(Pauli et al., 2005)

Expression of so^Scer\UAS.cPa under the control of Scer\GAL4^so.10 or Scer\GAL4^so.10.TOYmt rescues the missing eyes of so¹ animals, but not the ocelli. Expression of so^Scer\UAS.cPa under the control of Scer\GAL4^{so.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 so^Scer\UAS.cPa under the control of Scer\GAL4^so.7 fully rescues the missing eyes of so¹ animals, and partially rescues the ocelli. Expression of so^Scer\UAS.cPa under the control of Scer\GAL4^{so.7.EY.TOYmt.1.2.5} does not rescue the missing eyes of so¹ animals but rescues the ocelli. Expression of so^Scer\UAS.cPa under the control of Scer\GAL4^so.7.TOYmt rescues the missing eyes of so¹ animals but does not rescue the ocelli. Expression of so^Scer\UAS.cPa under the control of Scer\GAL4^{so.7.EY+TOYmt.1-5} does not rescue the missing eyes or ocelli of so¹ animals.

(Punzo et al., 2002)

The neuronal array phenotype in the eye disc is rescued along the posterior and lateral but not the anterior portions of the disc by so^Scer\UAS.cPa expressed under the control of Scer\GAL4^dpp.blk1 (the region of rescue correlates well with the domain of Scer\GAL4^dpp.blk1 expression). More than 95% of adult homozygotes are completely eyeless. The most posterior region of the adult eye is rescued by so^Scer\UAS.cPa expressed under the control of Scer\GAL4^E132.

(Pignoni et al., 1997)

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

(Cheyette et al., 1994)

Images (1)

Holtzman, S. and Kaufman, T. (2013)

Mutant

Wild-type