Allele Dmel\so¹

General Information
Symbol	Dmel\so¹	Species	D. melanogaster
Name		FlyBase ID	FBal0015924
Feature type	allele	Associated gene	Dmel\so

Allele class	loss of function allele
Mutagen	spontaneous
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class	loss of function allele (Pignoni et al., 1997)
Mutagen	spontaneous (Heitzler et al., 1993, Cheyette et al., 1994)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference 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)
Cytology
Phenotypic Data
Phenotypic Class
	cell growth defective \| somatic clone (Kenyon et al., 2005) circadian rhythm defective (Helfrich-Forster et al., 2002) increased cell death (Dearborn and Kunes, 2004) neuroanatomy defective (Helfrich-Forster and Homberg, 1993, Malpel et al., 2002) viable (Cheyette et al., 1994, Kenyon et al., 2005) visible (Kumar et al., 2004, Punzo et al., 2002) visible \| recessive (Pignoni et al., 1997, Royet and Finkelstein, 1997) visual behavior defective (Heitzler et al., 1993)
Phenotype Manifest In
	Bolwig organ (Cheyette et al., 1994) cortex of medulla (Dearborn and Kunes, 2004) cuticle \| ectopic \| somatic clone (Kenyon et al., 2005) embryonic/larval optic stalk (Murakami et al., 2007) eye (Cheyette et al., 1994, Kumar et al., 2004, Choi and Benzer, 1994, Heitzler et al., 1993, Pignoni et al., 1997, Serikaku and O'Tousa, 1994, Helfrich-Forster et al., 2002, Punzo et al., 2002, Royet and Finkelstein, 1997) eye \| somatic clone (Kenyon et al., 2005) eye disc (Huang et al., 1998, Pignoni et al., 1997, Anderson et al., 2006) eye disc \| somatic clone (Kenyon et al., 2005, 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 neuropil (Dearborn and Kunes, 2004) morphogenetic furrow \| somatic clone (Pignoni et al., 1997) ocellus (Cheyette et al., 1994, Choi and Benzer, 1994, Heitzler et al., 1993, Helfrich-Forster et al., 2002, Punzo et al., 2002) ommatidium (Huang et al., 1998, Kunes et al., 1993) optic lobe (Malpel et al., 2002, Helfrich-Forster et al., 2002) Pdf neuron (Helfrich-Forster and Homberg, 1993) retina (Anderson et al., 2006) subretinal glial cell (Hummel et al., 2002, Choi and Benzer, 1994) visual primordium (Cheyette et al., 1994)
Detailed Description
	Statement Reference Eye disc size in so[1] mutant clones is similar to wild type. (Wang and Sun, 2012) 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 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 the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement Reference so¹ has circadian rhythm defective phenotype, enhanceable by cry^b (Helfrich-Forster et al., 2002) so¹ has circadian rhythm defective phenotype, enhanceable by gl^60j (Helfrich-Forster et al., 2002)
Enhancer of
Statement Reference so¹ is an enhancer of visible phenotype of H^Scer\UAS.cMa/H^Scer\UAS.cMa, Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF (Mueller et al., 2005)
Other
Statement Reference Scer\GAL4^dpp.blk1, so¹, toy^Scer\UAS.cCa has visible phenotype (Niimi et al., 1999, 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 cell phenotype, enhanceable by gish¹ (Hummel et al., 2002)
Enhancer of
Statement Reference so¹ is an enhancer of eye phenotype of H^Scer\UAS.cMa/H^Scer\UAS.cMa, Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF (Mueller et al., 2005) so¹ is an enhancer of photoreceptor cell 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, ey^Scer\UAS.cHa, so¹ has leg phenotype (Halder et al., 1998, Halder et al., 1998) Scer\GAL4^dpp.blk1, ey^Scer\UAS.cHa, so¹ has wing disc phenotype (Halder et al., 1998, Halder et al., 1998) Scer\GAL4^dpp.blk1, so¹, toy^Scer\UAS.cCa has eye \| ectopic phenotype (Niimi et al., 1999, Niimi et al., 1999)
Additional Comments
Genetic Interactions
Statement Reference 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
Complementation & Rescue Data
Rescued by	so¹ is rescued by so^G66A.hs (Kenyon et al., 2005) so¹ is rescued by so^hs.PC (Cheyette et al., 1994) so¹ is rescued by so^Scer\UAS.cPa/Scer\GAL4^hs.PB (Kenyon et al., 2005) so¹ is rescued by so^so10-soAE.hs (Pauli et al., 2005)
Partially rescued by	so¹ is partially rescued by so^Scer\UAS.cPa/Scer\GAL4^dpp.blk1 (Pignoni et al., 1997) so¹ is partially rescued by so^Scer\UAS.cPa/Scer\GAL4^{so.7.EY.TOYmt.1.2.5} (Punzo et al., 2002) so¹ is partially rescued by so^Scer\UAS.cPa/Scer\GAL4^so.7.TOYmt (Punzo et al., 2002) so¹ is partially rescued by so^Scer\UAS.cPa/Scer\GAL4^so.7 (Punzo et al., 2002) so¹ is partially rescued by so^Scer\UAS.cPa/Scer\GAL4^{so.10.EY.TOYmt.1.2.5} (Punzo et al., 2002) so¹ is partially rescued by so^Scer\UAS.cPa/Scer\GAL4^so.10.TOYmt (Punzo et al., 2002) so¹ is partially rescued by so^Scer\UAS.cPa/Scer\GAL4^so.10 (Punzo et al., 2002) so¹ is partially rescued by so^Scer\UAS.cPa/Scer\GAL4^upd-E132 (Pignoni et al., 1997) so¹ is partially rescued by so^so11-soAE (Blanco et al., 2010)
Not rescued by	so¹ is not rescued by so^{L257P.Scer\UAS}/Scer\GAL4^hs.PB (Kenyon et al., 2005) so¹ is not rescued by so^Scer\UAS.cPa/Scer\GAL4^{so.7.EY+TOYmt.1-5} (Punzo et al., 2002) so¹ is not rescued by so^Scer\UAS.cPa/Scer\GAL4^{so.10.EY+TOYmt.1-5} (Punzo et al., 2002)
Comments	Expression of so[so11-soAE] rescues the eyeless and partially rescues the ocelliless phenotypes of so[1]. (Blanco et al., 2010) 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)
Stocks ( 2 )
Bloomington	401 so¹
Kyoto	105892 so¹
Notes on Origin
Discoverer	Milani, 1939.

Comments
	No interaction with P{sev-svp1} or P{sev-svp2} exists. (Begemann et al., 1995) Mutant phenotype can be rescue by introduction of P{hsp70/so} and heat pulses during eye-antennal imaginal disc development. (Serikaku and O'Tousa, 1994)
External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 2 )
Reported As
Symbol Synonym	so¹ (Zhang et al., 2006, Anderson et al., 2006, Murakami et al., 2007, Wang et al., 2008, Levine et al., 1997, Blanco et al., 2010, Wang and Sun, 2012) SO¹ (Kenyon et al., 2005)
Name Synonym
Secondary FlyBase IDs

References ( 47 )

Generate a list of	All references relating to this allele ( 47 )

List References by type	Research paper ( 43 ) Review ( 3 ) Abstract ( 1 )
Recent research papers ( 1 )
	Wang and Sun, 2012, Development 139(18): 3413--3421 Segregation of eye and antenna fates maintained by mutual antagonism in Drosophila. [FBrf0219201] Show all research papers ...
Recent reviews (0)
	All reviews listed in FlyBase were published before 2011 Show reviews ...

Allele Dmel\so1

Allele Dmel\so¹