|Feature type||allele||Associated gene||Dmel\aos|
|Also Known As||argosΔ7, argosIΔ7, argoslΔ7, aosd7, argosdelta7, argos1Δ7|
|Allele class||amorphic allele - genetic evidence, loss of function allele|
|Mutagen||Delta2-3, P-element activity|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Excision of a P-element causing deletion of the first exon encoding the putative ATG start codon and signal sequence.
|Phenotype Manifest In|
Virtually all eggs derived from egg chambers containing complete homozygous follicle cell clones appear normal and have two dorsal appendages.
argos[Δ7]/argos, argos[Δ7]/argos[W11] and argos[Δ7]/argos[p1] flies have blisters in the eye. Eggs derived from females with mosaic argos[Δ7] egg chambers have the normal number of two dorsal appendages. Only 5% of eggs derived from argos[Δ7]/argos[W11] 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 argos[Δ7] homozygous embryos have more oenocytes per cluster than wild-type. Unlike rho[Scer\UAS.cdCa]; Scer\GAL4[en-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.
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.
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.
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 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.
|NOT Enhancer of|
|NOT Suppressor of|
aos[+], aosΔ7, AckK156A.Scer\UAS, Scer\GAL4GMR.PU is a non-suppressor of visible phenotype of WAla5.GMR
|Phenotype Manifest In|
aosΔ7 has abdominal lateral pentascolopidial chordotonal organ lch5 | supernumerary phenotype, enhanceable by salmunspecified
aosΔ7 has dorsal acute muscle | precursor | ectopic phenotype, suppressible by Scer\GAL4twi.PB/EgfrDN.Scer\UAS
aosΔ7 has dorsal oblique muscle | ectopic phenotype, suppressible by Scer\GAL4twi.PB/EgfrDN.Scer\UAS
aosΔ7 has dorsal oblique muscle | precursor | ectopic phenotype, suppressible by Scer\GAL4twi.PB/EgfrDN.Scer\UAS
aos[+]/aosΔ7 is an enhancer of wing vein | ectopic phenotype of Scer\GAL4tub.PU, cswN308D.Scer\UAS.P\T
aosΔ7/Scer\GAL4tub.PU is an enhancer of wing vein phenotype of Scer\GAL4tub.PU, cswY279C.Scer\UAS.P\T
aosΔ7 is an enhancer of abdominal lateral pentascolopidial chordotonal organ lch5 | supernumerary phenotype of salmunspecified
aosΔ7 is an enhancer of photoreceptor cell R7 phenotype of CblDv.Scer\UAS, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF
aosΔ7 is an enhancer of wing vein | ectopic phenotype of CblDv.Scer\UAS, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF
|NOT Enhancer of|
aosΔ7 is a non-enhancer of chemosensory ventral triple row & microchaeta | ectopic phenotype of ed4.12
|NOT Suppressor of|
aosΔ7/aosΔ7 is a non-suppressor of photoreceptor cell R1 | somatic clone | third instar larval stage phenotype of raspT392
aosΔ7/aosΔ7 is a non-suppressor of photoreceptor cell R2 | somatic clone | third instar larval stage phenotype of raspT392
aosΔ7/aosΔ7 is a non-suppressor of photoreceptor cell R3 | somatic clone | third instar larval stage phenotype of raspT392
aosΔ7/aosΔ7 is a non-suppressor of photoreceptor cell R4 | somatic clone | third instar larval stage phenotype of raspT392
aosΔ7/aosΔ7 is a non-suppressor of photoreceptor cell R5 | somatic clone | third instar larval stage phenotype of raspT392
aosΔ7/aosΔ7 is a non-suppressor of photoreceptor cell R6 | somatic clone | third instar larval stage phenotype of raspT392
aosΔ7/aosΔ7 is a non-suppressor of photoreceptor cell R7 | somatic clone | third instar larval stage phenotype of raspT392
aosΔ7 is a non-suppressor of chemosensory ventral triple row & microchaeta | ectopic phenotype of ed4.12
Heterozygosity for aos[Δ7] does not suppress the small eye phenotype caused by W[Ala5.GMR]. Expression of Ack[K156A.Scer\UAS] under the control of Scer\GAL4[GMR.PU] in conjunction with aos[Δ7]/+ does not suppress the small eye phenotype caused by W[Ala5.GMR]. Expression of Ack[Scer\UAS.cSb] under the control of Scer\GAL4[GMR.PU] suppresses the small eye phenotype caused by W[Ala5.GMR]. Further suppression is seen if the flies are also heterozygous for aos[Δ7]/+. Animals expressing Ack[Scer\UAS.cSb] under the control of Scer\GAL4[GMR.PU] in a aos[Δ7]/+ background show a 25% increase in pigment cell number when assessed at 42% pupa development.
One copy of aos[Δ7] enhances the reduction in wing blade area seen in homozygous sl males. One copy of aos[Δ7] significantly enhances the ectopic wing vein phenotype seen in sl homozygotes. One copy of aos[Δ7] dramatically enhances the percentage of sl mutant ommatidia that contain extra R7 photoreceptors. The eyes also appear rougher than in sl mutants alone.
One copy of aos[Δ7] enhances the extra wing vein phenotype seen in sty[S73] heterozygotes at 29[o]C. One copy of aos[Δ7] enhances the extra vein phenotype seen in rho-5[KO1] sty[S73] double heterozygotes at 29[o]C.
The rough-eye phenotype observed in Fas2[EB112]/Fas2[e76] flies is enhanced by the presence of argos[Δ7]/+.
The presence of a argos[Δ7] background significantly enhances ectopic wing vein formation found in csw[Y279C.Scer\UAS] (Scer\GAL4[tub]) mutants.
The loss of photoreceptor cells seen in homozygous mop[T612] clones in the eye disc is not rescued if the clones are also homozygous for argos[Δ7].
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.
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 argos[Δ7] background enhances the eye and wing vein phenotype of Scer\GAL4[GMR.PF] Cbl[Dv.Scer\UAS] mutants.
|Complementation & Rescue Data|
|Fails to complement|
|Partially rescued by|
|Not rescued by|
|Stocks ( 2 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 16 )|
(Voas and Rebay, 2003, Rawlins et al., 2003, Alvarez et al., 2003, Carmena et al., 2002, Yang and Baker, 2001, Shandala et al., 1999, Simcox, 1997, Tyler et al., 2007, Alvarado et al., 2006, Miura et al., 2006, Miura et al., 2008, Lachance et al., 2009, Oishi et al., 2009, Murillo-Maldonado et al., 2011, Oishi et al., 2006)
|Secondary FlyBase IDs|
|References ( 62 )|
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|Recent research papers ( 5 )|