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General Information
Symbol
Dmel\aosΔ7
Species
D. melanogaster
Name
FlyBase ID
FBal0043093
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
argosIΔ7, argosΔ7, argoslΔ7, argosdelta7, aosd7, argos1Δ7, arg1Δ7, aoslΔ7
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Cytology
Nature of the lesion
Statement
Reference

Excision of the P{lwB} element.

Excision of a P-element causing deletion of the first exon encoding the putative ATG start codon and signal sequence.

Deletion caused by imprecise excision of the P{lwB} element of argosW11. Deletion removes the 5' exon and the beginning of the major open reading frame.

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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

The neuroepithelium of aosΔ7 L3 larvae is overgrown compared to wild type. In the subsequent stage, ectopic and precocious neuroblasts are scattered throughout this enlarged neuroepithelium.

Virtually all eggs derived from egg chambers containing complete homozygous follicle cell clones appear normal and have two dorsal appendages.

argosΔ7/+ flies have normal eyes at 20[o]C.

argosΔ7/argos257, argosΔ7/argosW11 and argosΔ7/argosp1 flies have blisters in the eye.

Eggs derived from females with mosaic argosΔ7 egg chambers have the normal number of two dorsal appendages.

Only 5% of eggs derived from argosΔ7/argosW11 females have defects in dorsal appendage morphology, which include a reduced distance between the two appendages and appendages that are shorter than normal.

argosΔ7/Df(3L)Exel6129 flies have eyes with a roughened appearance and prominent blistering along the posterior margin.

argosΔ7 clones in the eye disc induce the formation of extra photoreceptor cells; 46.2% of ommatidia within these clones have 8 photoreceptor cells, 40.7% of ommatidia have 9, 11.1% have 10 and 1% have 11.

Stage 15 argosΔ7 embryos have ~36 genital disc precursor cells, while wild type embryos have only 22 at this stage.

Stage 16 argosΔ7 homozygous embryos have more oenocytes per cluster than wild-type. Unlike rhoScer\UAS.cdCa; Scer\GAL4en-e16E the oenocyte clusters in these embryos do not show a multi-modal distribution of cell numbers with peaks corresponding to multiples of 3. Analysis of larval oenocyte precursor delamination shows that it occurs continuously rather than in widely spaced cycles with 3 delaminating cells per cycle as seen in wild-type. In the resulting oenocyte clusters terminal differentiation of some oenocytes is blocked or delayed.

argosrlt/argosΔ7 animals exhibit a ommatidial rotation phenotype.

63% of ommatidia in argosΔ7/argosA254Δ15 animals exhibit extra R cells. Of those that ommatidia that remain about 47% exhibit misrotations, about 10% exhibit achirality, and about 4% exhibit the wrong chirality. About 43% of ommatidia in argosΔ7/argos5F4 animals exhibit extra R cells. Of those that ommatidia that remain about 45% exhibit misrotations, about 5% exhibit achirality, and none exhibit the wrong chirality. About 11% of ommatidia in argosΔ7/argosrlt animals exhibit extra R cells. Of those that ommatidia that remain about 52% exhibit misrotations, about 1% exhibit achirality, and about 1% exhibit the wrong chirality. Of the misrotated ommatidia just less than half are underrotated.

In argos5F4/argosΔ7 transheterozygotes 45% of adult ommatidia have extra photoreceptors. Many of the ommatidia with a normal complement of photoreceptor cells have polarity defects up to 59% of ommatidia are misrotated, while only 5% appear achiral and usually less than 1% have the wrong chirality. It appears that a transformation of mystery cells to photoreceptor R3/R4 is the cause of the extra photoreceptor cells. When the eye discs of these mutants are examined about 60% of immature clusters exhibit extra photoreceptor precursor cells. In row 7-8 the number of extra cells decreases to about 25%. In the adult only about 15% of clusters have ectopic R3/R4 cells.

argosΔ7/argos05845 escaper adults have extensive blistering along the posterior edge of the eye.

Extra EPCs (eve-positive heart associated or pericardial cells) and DA1 and DO2 founders (and subsequently muscles) are seen in mutant embryos. Additional founders of the P2 and p15 lineages of the developing embryonic mesoderm are seen.

Homozygous clones in the adult abdomen do not show any consistent alterations of normal polarity.

Ommatidial spacing is not affected in argosΔ7 somatic clones in the eye, even in very large clones.

The number of chordotonal organs in the lateral cluster is increased from 5 to 6 in mutant embryos. In stage 11 embryos, the oenocyte precursor whorl is enlarged and contains many extra cells and by stage 16 oenocyte clusters containing 15-27 cells are seen.

Homozygous clones in the eye disc that include several ommatidia show no defects in R8 precursor specification. Positioning of R8 precursors is unaffected by mutant cells in posterior columns. In larger clones that are more than 10 ommatidia wide the pattern of R8 specification is disrupted.

Heterozygotes show a quantitative effect on wing shape in intervein regions C and D compared to wild type.

Mutant embryos show a 'cyclops' phenotype in which the optic lobes are enlarged and show dorsal fusion.

Homozygous embryos have missing or malformed H-piece structures.

At stage 16 optic lobes are enlarged and fused. Frontal and hypocerebral ganglion are enlarged and the recurrens nerve is thickened.

Germline clones fail to rescue the female sterile phenotype of Fs(3)Apc.

Germline clones reveal no requirement for argos in the oocyte in patterning the egg, or in the viability or patterning of the embryo. Follicle cell clones cause a fused dorsal appendage phenotype. Larvae hatch from the eggs, with dorsal-ventral pattern unperturbed. argosΔ7/argosW11 hypomorphic females lay a significant proportion of eggs with fused dorsal appendages.

Abnormal CNS axon pattern phenotype. An increase in number of midline glia and lateral chordotonal organs is also observed.

argosΔ5/argosΔ7 embryos exhibit expansion of the denticle belts. Wing, leg, haltere and eye/antenna argosΔ5/argosΔ7 mutant discs can be in vivo cultured.

The number of midline glia cells is increased to an average of 5.3 +/- 0.2 cells per segment in homozygous embryos.

Additional small denticles are often found located anteriorly to the abdominal denticle belts in homozygous embryos, in the most extreme cases forming a complete additional row anterior to row 1. Extra small denticles are also found in row 6, resulting in a slightly higher density of denticles compared to wild-type.

Transheterozygotes with Df(3L)st-g18 die before hatching. Transheterozygotes with Df(3L)st-k7 or Df(3L)st-f13 have rare escapers, adult survivors develop a characteristic eye phenotype, bulging of the posterior part of the eye that spreads into the anterior part.

Homozygous clones in the eye cause extra outer photoreceptors, severity of the phenotype depends on the size of the clone. Homozygotes display severe disruption and broadening of the embryonic head skeleton, broadening of the ventral epidermis as shown by increased distance between the Keilin's organs.

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

aos[+]/aosΔ7, styS73 has visible | dominant phenotype, enhanceable by rho-5[+]/rho-5KO1

Enhancer of
Statement
Reference

aos[+]/aosΔ7 is an enhancer of visible phenotype of Chmp1GD11219, Scer\GAL4Bx-MS1096

aos[+]/aosΔ7 is an enhancer of visible | dominant phenotype of Snr1E1

aos[+]/aosΔ7 is an enhancer of size defective | adult stage phenotype of sl2

aos[+]/aosΔ7 is an enhancer of visible | adult stage phenotype of sl2

aos[+]/aosΔ7 is an enhancer of visible | dominant phenotype of styS73

aos[+]/aosΔ7 is an enhancer of visible | dominant phenotype of rho-5[+]/rho-5KO1, styS73

aos[+]/aosΔ7 is an enhancer of visible phenotype of DgdsRNA.UAS, Scer\GAL4Tub.PU

aos[+]/aosΔ7 is an enhancer of visible phenotype of Scer\GAL4Tub.PU, cswN308D.UASp

aosΔ7/argos[+] is an enhancer of planar polarity defective | recessive phenotype of sl9

aosΔ7, argos[+], N[+], N55e11 is an enhancer of planar polarity defective phenotype of Pcyt116919

aosΔ7 is an enhancer of visible phenotype of bul1

NOT Enhancer of
Statement
Reference

aosΔ7/argos[+] is a non-enhancer of planar polarity defective phenotype of Pcyt116919

Suppressor of
Statement
Reference

aos[+], aosΔ7, AckUAS.cSb, Scer\GAL4GMR.PU is a suppressor of visible phenotype of hidAla5.GMR

aos[+]/aosΔ7 is a suppressor of visible phenotype of DysdsRNA.NH2.UAS, Scer\GAL4Act.PU

aosΔ7 is a suppressor of lethal phenotype of hidhs.PG

aosΔ7 is a suppressor of visible phenotype of bulD

NOT Suppressor of
Statement
Reference

aos[+]/aosΔ7 is a non-suppressor of visible phenotype of hidAla5.GMR

aos[+], aosΔ7, AckK156A.UAS, Scer\GAL4GMR.PU is a non-suppressor of visible phenotype of hidAla5.GMR

aosΔ7 is a non-suppressor of decreased cell death phenotype of Ras85DR68Q

Other
Statement
Reference
Phenotype Manifest In
Enhanced by
Statement
Reference
Suppressed by
Enhancer of
Statement
Reference

aos[+]/aosΔ7 is an enhancer of wing vein | ectopic phenotype of Snr1E1

aos[+]/aosΔ7 is an enhancer of wing blade phenotype of sl2

aos[+]/aosΔ7 is an enhancer of wing vein | ectopic phenotype of sl2

aos[+]/aosΔ7 is an enhancer of eye phenotype of sl2

aos[+]/aosΔ7 is an enhancer of wing vein phenotype of styS73

aos[+]/aosΔ7 is an enhancer of wing vein phenotype of rho-5[+]/rho-5KO1, styS73

aosΔ7 is an enhancer of eye phenotype of Fas2EB112/Fas2e76

aos[+]/aosΔ7 is an enhancer of wing vein | ectopic phenotype of Scer\GAL4Tub.PU, cswN308D.UASp

aosΔ7/argos[+] is an enhancer of photoreceptor cell R7 | supernumerary phenotype of sl9

aosΔ7/argos[+] is an enhancer of ommatidium phenotype of sl9

aosΔ7/argos[+] is an enhancer of interommatidial bristle phenotype of sl9

aosΔ7/argos[+] is an enhancer of photoreceptor cell R8 | supernumerary phenotype of ed4.12

aosΔ7 is an enhancer of ommatidium phenotype of fz20/fz19

aosΔ7/argos[+] is an enhancer of ommatidium phenotype of Ras85DV12.sev

aosΔ7/argos[+] is an enhancer of eye phenotype of Ras85DV12.sev

aosΔ7, argos[+], N[+], N55e11 is an enhancer of eye photoreceptor cell phenotype of Pcyt116919

aosΔ7, argos[+], N[+], N55e11 is an enhancer of ommatidium phenotype of Pcyt116919

aosΔ7 is an enhancer of pericardial cell | ectopic phenotype of DlX

aosΔ7 is an enhancer of pericardial cell | precursor | ectopic phenotype of DlX

aosΔ7 is an enhancer of dorsal acute muscle | ectopic phenotype of DlX

aosΔ7 is an enhancer of eye phenotype of bul1

NOT Enhancer of
Statement
Reference

aosΔ7 is a non-enhancer of chemosensory ventral triple row & microchaeta | ectopic phenotype of ed4.12

aosΔ7 is a non-enhancer of dorsal triple row & microchaeta | ectopic phenotype of ed4.12

aosΔ7 is a non-enhancer of dorsocentral bristle | ectopic phenotype of ed4.12

aosΔ7 is a non-enhancer of scutellar bristle | ectopic phenotype of ed4.12

aosΔ7/argos[+] is a non-enhancer of eye photoreceptor cell phenotype of Pcyt116919

aosΔ7/argos[+] is a non-enhancer of ommatidium phenotype of Pcyt116919

aosΔ7/argos[+] is a non-enhancer of wing phenotype of N55e11

Suppressor of
Statement
Reference

aos[+], aosΔ7, AckUAS.cSb, Scer\GAL4GMR.PU is a suppressor of eye phenotype of hidAla5.GMR

aosΔ7 is a suppressor of ommatidium phenotype of Ras64BV14.Act5C

aosΔ7 is a suppressor of eye phenotype of armS56F.GMR

aosΔ7 is a suppressor of eye phenotype of hidGMR.PG/WGMR.PG

aosΔ7 is a suppressor of ommatidium phenotype of hidGMR.PG/WGMR.PG

aosΔ7 is a suppressor of eye phenotype of bulD

NOT Suppressor of
Statement
Reference

aos[+]/aosΔ7 is a non-suppressor of eye phenotype of hidAla5.GMR

aos[+], aosΔ7, AckK156A.UAS, Scer\GAL4GMR.PU is a non-suppressor of eye phenotype of hidAla5.GMR

aosΔ7 is a non-suppressor of wing vein | ectopic phenotype of Ras85DR68Q

aosΔ7 is a non-suppressor of eye phenotype of Ras85DR68Q

aosΔ7 is a non-suppressor of midline glial cell phenotype of Ras85DR68Q

aosΔ7 is a non-suppressor of ommatidium phenotype of Ras85DR68Q

aosΔ7 is a non-suppressor of wing phenotype of Ras85DR68Q

aosΔ7 is a non-suppressor of posterior crossvein phenotype of Ras85DR68Q

aosΔ7 is a non-suppressor of crossvein phenotype of Ras85DR68Q

aosΔ7 is a non-suppressor of wing vein L4 phenotype of Ras85DR68Q

aosΔ7 is a non-suppressor of wing vein L5 phenotype of Ras85DR68Q

aosΔ7 is a non-suppressor of chemosensory ventral triple row & microchaeta | ectopic phenotype of ed4.12

aosΔ7 is a non-suppressor of dorsal triple row & microchaeta | ectopic phenotype of ed4.12

aosΔ7 is a non-suppressor of dorsocentral bristle | ectopic phenotype of ed4.12

aosΔ7 is a non-suppressor of scutellar bristle | ectopic phenotype of ed4.12

Other
Additional Comments
Genetic Interactions
Statement
Reference

aosΔ7 dominantly enhances the increased differentiating germ cell phenotype in goe5-11/goe331 mutant larval ovaries.

While neither goe5-11/goe331 nor aosΔ7/+ ovaries exhibit a remarkable reduction in the number of germline stem cells (GSCs) at white pupal stage, establishment is severely impaired in goe5-11/goe331; aosΔ7/+ ovaries. This reduction in GSC number is likely the result of an insufficient primordial germ cell pool, because both ovariole formation and niche development occur normally in goe5-11/goe331; aosΔ7/+ ovaries.

An aosΔ7 mutant background does not alter the ommatidial rotation phenotype seen in flies expressing miple1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4hs.2sev.

An aosΔ7 mutant background enhances the eye roughness seen in flies expressing miple1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4GMR.PU.

Heterozygosity for aosΔ7 does not suppress the small eye phenotype caused by WAla5.GMR.

Expression of AckK156A.Scer\UAS under the control of Scer\GAL4GMR.PU in conjunction with aosΔ7/+ does not suppress the small eye phenotype caused by WAla5.GMR.

Expression of AckScer\UAS.cSb under the control of Scer\GAL4GMR.PU suppresses the small eye phenotype caused by WAla5.GMR. Further suppression is seen if the flies are also heterozygous for aosΔ7/+.

Animals expressing AckScer\UAS.cSb under the control of Scer\GAL4GMR.PU in a aosΔ7/+ background show a 25% increase in pigment cell number when assessed at 42% pupa development.

One copy of aosΔ7 enhances the reduction in wing blade area seen in homozygous sl2 males.

One copy of aosΔ7 significantly enhances the ectopic wing vein phenotype seen in sl2 homozygotes.

One copy of aosΔ7 dramatically enhances the percentage of sl2 mutant ommatidia that contain extra R7 photoreceptors. The eyes also appear rougher than in sl2 mutants alone.

One copy of aosΔ7 enhances the extra wing vein phenotype seen in styS73 heterozygotes at 29[o]C.

One copy of aosΔ7 enhances the extra vein phenotype seen in rho-5KO1 styS73 double heterozygotes at 29[o]C.

The rough-eye phenotype observed in Fas2EB112/Fas2e76 flies is enhanced by the presence of argosΔ7/+.

The presence of a argosΔ7 background significantly enhances ectopic wing vein formation found in cswY279C.Scer\UAS (Scer\GAL4tub) mutants.

One copy of aosΔ7 strongly suppresses the detached posterior crossvein phenotype seen when DysdsRNA.NH2.Scer\UAS is expressed under the control of Scer\GAL4Act.PU but produces extra wing vein material.

One copy of aosΔ7 enhances the posterior crossvein phenotype seen when DgdsRNA.Scer\UAS is expressed under the control of Scer\GAL4tub.PU.

The loss of photoreceptor cells seen in homozygous mopT612 clones in the eye disc is not rescued if the clones are also homozygous for argosΔ7.

argosΔ7 does not protect Df(1)su(s)R194/+ clones in the eye; Df(1)su(s)R194/+ ; argosΔ7 clones are not recovered in the adult eye in animals with mosaic eyes containing two genotypes of cells with respect to RpL36; cells which are Df(1)su(s)R194/+ and cells in which the haplo-insufficiency of Df(1)su(s)R194/+ for RpL36 has been rescued by RpL36+t4 (in a wild-type background the Df(1)su(s)R194/+ clones are eliminated by cell competition and are not seen in the adult eye in these animals). Also, argosΔ7 does not prevent apoptosis of Df(1)su(s)R194/+ cells in the wing.

argosΔ7 styΔ5 Minute clones in the eye disc form large, disorganised clusters in the morphogenetic furrow compared to the clusters formed in wild-type eye discs.

The extra photoreceptor cell phenotype of argosΔ7 clones is enhanced in argosΔ7 Gug14967 clones, with a greater percentage of ommatidia showing supernumerary photoreceptor cells. These extra photoreceptor cells are never R8 cells. In contrast, ru1 rho7M43 Gug14967 argosΔ7 mutant clones lack photoreceptor cells.

The ed4.12 R8 cell twinning phenotype is strongly enhanced by argosΔ7/+.

argosΔ7/+ mildly enhances the edk01102 phenotype; the number of ommatidia with multiple R8 cells is increased from 18% to 34% in the double mutant flies.

The addition of argosΔ7/+ enhances the eye cell polarity phenotype seen in fz19/fz20 animals. Heterozygotes suppress the ommatidial polarity defects seen in Ras64BV14.Act5C.

The eye blistering phenotype seen in argosΔ7/argos05845 escaper adults is enhanced by rno3/+, so that it covers much of the eye. The rough eye phenotype of Ras85DV12.sev flies is enhanced by argosΔ7/+.

The notching seen in wings of N55e11/+ flies is not enhanced in argosΔ7/+ mutants. While Cct116919/+, argosΔ7/+ double heterozygotes have no eye defects, N55e11/+; Cct116919/+, argosΔ7/+ triple heterozygotes show an enhancement in the defective eye phenotype (loss of photoreceptor cells, defects in ommatidial polarity and chirality and a partial loss of the ventral eye) seen in Cct116919 mutants.

The EPC and DA1 phenotype seen in argosΔ7 and DlX exhibit a synergistic effect on each other when combined. An increase in the number of DO2 muscles is also seen.

salmunspecified argosΔ7 double mutant embryos have a dramatic chordotonal organ overproduction phenotype that is more severe than that seen in either single mutant. 9 or more lateral chordotonal organs per hemisegment are frequently seen, that are often (as in salmunspecified single mutants) scattered in lateral and dorsal positions. The double mutant embryos lack oenocytes.

A argosΔ7 background enhances the eye and wing vein phenotype of Scer\GAL4GMR.PF CblDv.Scer\UAS mutants.

styS73/argosΔ7 double heterozygotes have a mild rough eye phenotype.

Transheterozygotes with bulbp are semi-lethal, surviving adults display an eye phenotype.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
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Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (16)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (73)