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General Information
Symbol
Dmel\ato1
Species
D. melanogaster
Name
FlyBase ID
FBal0034197
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
ato1
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

G8278198A

Amino acid change:

A25T | ato-PA

Reported amino acid change:

A25T

Comment:

One of three predicted amino acid changes in the mutant relative to the parent chromosome.

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

point mutation
Nucleotide change:

G8278884Y

Amino acid change:

K253N | ato-PA

Reported amino acid change:

K253N

Comment:

One of three predicted amino acid changes in the mutant relative to the parent chromosome.

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

point mutation
Nucleotide change:

A8278907T

Amino acid change:

N261I | ato-PA

Reported amino acid change:

N261I

Comment:

One of three predicted amino acid changes in the mutant relative to the parent chromosome.

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Deficient in the DNA binding domain.

Amino acid replacement: N261I. Amino acid replacement: K253N. Amino acid replacement: A25T. Mutations are in a motif of the basic domain (N261I), a short distance proximally on the edge of the basic domain (K253N) and near the N terminus respectively (A25T).

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

antenna & neuron

antennal segment 3 & fascicle (with Df(3R)p13)

eye photoreceptor cell & axon (with ato2)

glial cell & antenna (with Df(3R)p13)

glial cell & antennal lobe (with Df(3R)p13)

interneuron & antennal lobe (with Df(3R)p13)

morphogenetic furrow & filopodium | somatic clone

olfactory neuron & embryonic antennal sense organ

pioneer neuron & adult antennal nerve & pupa (with Df(3R)p13)

sensory mother cell & antennal disc

Detailed Description
Statement
Reference

ato1/ato1 mutant adults and ato1/ato1 somatic clones in the optic lobe of third instar larvae have a significantly decreased number of T4/T5 neurons compared to wild-type controls. In larvae, somatic clones which are located in the neural compartment of the optic lobe contain T4/T5 neurons displaying signs of dedifferentiation.

In the optic lobe of ato1/ato1 third instar larvae a significantly increased number of type III neuroblasts become polarized (determined by distribution of mira) and exhibit an increase in cell size.

ato1/ato1 larvae contain a well differentiated VA cell in 46% of segments, in the complete absence of ventral ChOs.

In olfactory preference assays for polyamines, ato1/ato1 flies do not show a preference for putrescine or cadaverine, in contrast to wild type flies which do show a preference for these compounds.

In ato1/Df(3R)p13 adult flies, antennal lobe structure is disrupted, with disorganized glomeruli lacking obvious borders. Axons of amos-positive olfactory receptor neurons Or67d and Or47b fail to cross the midline and do not form the commissure, are misrouted and some accumulate outside of the antennal lobe.

The neurites of developing homozygous ato1 T4/T5 neuron clones show defects in third instar larvae, showing over-fasciculation (36% penetrance), and guidance (64%) and growth (48%) defects.

ato1 mutants lack Cho neurons and a subset of multiple dendritic (md) neurons. These mutants do not exhibit an electrophysiological response to sound.

ato1/ato1090 mutants exhibit a small, rough eye phenotype at 25[o]C.

ato1/Df(3R)p13 flies lack the Johnston's organ.

Hemizygous ato1/Df(3R)p13 escapers are nearly or completely eyeless, displaying only a few ommatidia when eye tissue is present.

Adult ato1 flies show uncoordinated behaviour. They have a dramatically reduced climbing ability in bang tests compared with wild type controls.

Mutant larvae do not show a normal response to vibration, showing a small decrease in crawling speed with no head turning.

The total number of oenocytes that form is significantly decreased in ato1 mutant embryos as compared to controls. Control embryos have clusters of approximately six oenocytes in each of seven abdominal segments. In contrast, many segments of ato1 mutant embryos completely lack oenocytes. When oenocytes do develop in ato1 mutants, fewer of them form than in control segments.

90.5% of abdominal segments contain an lch5 neuron in ato1 homozygous embryos.

Mutants show no response to an auditory stimulus mimicking flies' courtship song.

Transheterozygous ato1090/ato1 mutants produce small rough eyes at 25[o]C.

The number of neurons in the dorsal organ ganglion are reduced in mutant embryos compared to wild type. The number of olfactory receptor neurons in the DO ganglion is reduced in the mutant embryos (average number is 8 compared to the wild-type number of 21).

ato1 Minute clones in the eye disc fail to form the arcs and rosettes of cells in the morphogenetic furrow that are seen in wild-type eye discs.

ato1/Df(3R)p13 embryos lack C1 chordotonal organ precursor cells and have no larval oenocyte precursors.

In the adult olfactory system, ato specifies a subset of neurons that are the first to develop and appear to guide the rest of the axons into the lobe. In ato1/Df(3R)p13 animals, "pioneer" antennal sensory neurons fail to form and the remaining antennal sensory neurons stall at the entry to the olfactory lobe.

Morphogenetic furrow formation can occur in mutant eye discs and the furrow progresses anteriorly to a certain distance, although retinal differentiation fails to occur.

ato1/Df(3R)p13 mutant animals lack a large fraction of glia.

ato1/Df(3R)p13 larvae have reduced touch sensitivity compared to wild-type. Locomotion in these larvae is aberrant: compared to controls they are slower and they pause, turn and retreat more often. These defects in locomotion arise at least partially from defective peristaltic motion: maximum larval length, stride period and % positive and negative flow are all defective.

ato1/Df(3R)p13 flies have an eye that is a patch of pigment with few sensory hairs.

In the pupal antennal imaginal disc of mutant animals, the first and second waves of sensory organ precursor formation do not occur.

ato1/Df(3R)p13 embryos lack oenocytes.

The eyes of homozygotes are reduced to a slit of pigment cells.

Ommatidial clusters situated posterior to ato1 clones display over-rotation phenotypes at a high frequency. Cytoplasmic extensions, extending from the morphogenetic furrow into these clones, follow convoluted paths rather than being straight and aligned with each other as in wild-type.

ato1 mutants lack the Johnston's organ and the circular outline of the joint between antennal segments 2 and 3.

The mechanical response of the antenna to sound is severely affected in homozygous and ato1/Df(3R)p13 flies compared to wild-type controls. The response of the entire antenna to sound in homozygous and ato1/Df(3R)p13 flies is similar to that observed on the head capsule with respect to both its amplitude and frequency composition. Neither the funiculus nor the arista vibrate in a coherent manner with sound (in contrast to wild type), demonstrating that the entire antenna is immobile and stiff in the mutant animals.

Homozygous and ato1/Df(3R)p13 flies show anatomical defects in the antennal joints. The hook that is normally present at the proximal end of the funicular stalk is missing in the mutant animals, and the funicular stalk enters the pit of the pedicel only in part, connecting broadly to both the inner wall and the anterior edge of the pedicel. The V-shaped cuticular rims that are present on either side of the hook in cross-sections at the connection between the pedicel and funiculus in wild-type animals are missing in the mutant flies, and the thin joint membranes that surround the hook and the rims in wild-type flies are missing, with the intersegmental cuticle being constantly thick in the mutant flies.

Antennal nerves stall at the periphery of the olfactory lobe up until the mid-pupal stage in ato1/Df(3R)p13 animals, with only very few fibres projecting into the lobe. The antennal nerves do enter the olfactory lobe later in development, but they remain disorganised and no obvious glomerular structures are seen. The antennal commissure fails to form. Olfactory lobe associated interneurons are normal. The distribution of glial cells within the antennal lobe is normal, but the glial processes show excessive branching. The number of peripheral glia associated with the olfactory neurons in the antenna is reduced in ato1/Df(3R)p13 pupae and the 3 fascicle that are normally seen in wild-type animals are merged into a single bundle. Projection interneurons are present in the antennal lobes of ato1/Df(3R)p13 adults, but they are unpatterned, in contrast to wild type. ato1/Df(3R)p13 antenna completely lack coeloconic sensilla. ato1/ato2 antenna have a small number of coeloconic sensilla. The antennal lobes have normal glomeruli and the inter-antennal commissure is present. The elaboration of glial cell processes within the antennal lobe is normal.

ato1/Df(3R)p13 embryos have hemisegments in which the lch5 array is either completely missing or reduced to a single lateral chordotonal organ. Oenocyte formation is completely abolished in those segments lacking all lateral chordotonal organs. In the majority of cases where a single lateral chordotonal organ is formed, it is associated with an oenocyte cluster of normal or somewhat reduced cell number. Similar phenotypes are seen in ato1 homozygotes, although the phenotype is less penetrant.

Oenocytes do not form in homozygous embryos, where the formation of the primary sensory organ precursors (SOPs) is compromised in most segments. In segments where remnant SOPs do develop, oenocytes can develop.

Mutant males demonstrate vigorous courtship including courtship songs. 66% of mutant males use both of their wings simultaneously during courtship song production (in contrast to wild-type males which vibrate only one wing at a time). Relative amplitude of the sine song and pulse number is higher than normal in mutant males. Pulse duration is significantly longer than wild-type.

Mutant embryos lack all chordotonal neurons.

The second antennal segment is devoid of scolopidia. The antennal nerve is present. No sound evoked potential can be recorded from the antennal nerve.

The dorsal, ventral brain and ventral lobular clusters (that normally express ato) are present in homozygous and hemizygous brains. In third larval instar brains there are severe defects in dorsal cluster (DC) position and organisation, and the cells appear to be less tightly clustered then normal. The axons are clearly defasciculated. These defects are seen with about 15% penetrance. The DC axons form a commissural tract. In adult brains, in addition to the positioning defects of the DC, the arborisation pattern of the DC over the lobula is severely impaired in hemizygous flies. Most axons enter the lobula either ventrally or dorsally and show very limited branching, failing to form a proper "fan-shaped" pattern.

ato1/Df(3R)p13 animals show a striking change in fascicular pattern of sensory neurons and glia in the third antennal segment. While all three branches are identifiable, they exit the antenna in a single bundle rather than distinct fascicles. The aristal neurons also fail to form. The number of glial cells present along the exiting sensory projections is also significantly reduced. ato1/Df(3R)p13 animals also show a dramatic disorganisation of the antennal glomeruli. In most antennal lobes examined, no glomeruli can be discerned at all. In a few cases one or two glomeruli are apparent.

Photoreceptor development is aberrant in ato1 eye-antennal discs.

The eyes of ato1 mutant flies are totally devoid of ommatidia.

ato1/ato2 flies have severely reduced eyes, which nevertheless contain ommatidia (approximately 200-300 in males, 5-15 in females). The ommatidia mostly contain fewer photoreceptors than wild type. The photoreceptor clusters are variably reduced, containing from 1-8 photoreceptors and any or all of the recruited photoreceptors can be affected. Photoreceptor axons navigate to the optic stalk poorly. This axon pathfinding defect is more severe in females. Those axons that reach the optic stalk are able to continue to their target sites within the optic lobe. Homozygous flies lack the compound eye, since the ommatidial founder cells (R8 photoreceptors) are not selected in these animals.

Progression of the morphogenetic furrow is slightly delayed across homozygous clones in the eye.

Mutant embryos lack the Bolwig's organ.

No ommatidia are formed in the presumptive eye field of homozygous flies, except for a few pigment cells and bristles. Flies carrying one or two copies of atot5'eye show no rescue of the ato1 eye phenotype. Flies carrying one or two copies of both atot5'eye and atot3'F.5.8 show rescue of the ato1 eye phenotype; flies carrying one copy of each construct typically have eyes containing 40% of the normal number of ommatidia, while flies carrying two copies of each construct have almost wild-type eyes.

Hemizygous antenna lack all the sensilla coeloconica. Maxillary palps lack sensilla basiconica. Antenna sacculus is absent, instead a few sensilla basiconica are present. The axonal bundle 2 fails to emerge out of the third antennal segment. Loss of sc and ac does not affect the hemizygous phenotype.

ato1/Df(3R)p13 flies completely lack sensilla coelonica on the surface of the third antennal segment, while the numbers and morphology of the sensilla basiconica and trichodea are normal. The sacculus is missing.

In mutant embryos all chordotonal organs are absent except for one scolopidium of lch5.

The lateral five chordotonal organ (lch5) neurons are missing in each abdominal segment. Most of the lch5 neurons are restored in the thoracic segment T2 and the odd-numbered abdominal segments when atoScer\UAS.cCa is expressed in ato1 flies using Scer\GAL4h-1J3. ato::scbHLH.ato.Scer\UAS and ato::scb.ato.Scer\UAS restore many of the lch5 neurons in the odd-numbered abdominal segments A1 and A3 when expressed in ato1 flies using Scer\GAL4h-1J3. scScer\UAS.cCa does not rescue the ato1 mutant phenotype when expressed using Scer\GAL4h-1J3.

Embryos lack almost all chordotonal organs of the thorax and abdomen. The remaining PNS is largely unaffected. Mutant larvae can hatch and survive to adulthood. Adult flies lack chordotonal organs associated with femur, wing base or ventral abdomen, and also lack Johnston's organ. Flies are clumsy on their feet and attempt to fly only with extreme reluctance. Chordotonal organ precursors are clearly and specifically missing in the leg, wing and antennal discs. No photoreceptors form, though a partial morphogenetic furrow remains in the mutant eye discs. Extensive cell death occurs in the larval eye disc posterior to the morphogenetic furrow. BrdU incorporation studies suggest that the second round or replication, which occurs in wild type posterior to the morphogenetic furrow, only occurs in the mutant as long as the furrow is moving.

Homozygotes and hemizygotes are almost eyeless, compound eye is a small red patch with a smooth surface and a few ommatidial bristles, and also lack ocelli. Photoreceptors are completely absent and the optic lobe is reduced. Eye antennal disc from third instar larvae shows a remnant of the morphogenetic furrow and extensive cell death in regions posterior to this crease. X ray induced homozygous clones in developing eye discs of heterozygous larvae result in a scar due to absence of ommatidia.

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

ato1 has visible | recessive phenotype, suppressible | partially by amosRoi-1/amos[+]

ato1 has visible phenotype, suppressible | partially by scUAS.cCa/Scer\GAL47

ato1, atot5'eye has visible phenotype, suppressible | partially by sct3'F.5.8

ato1, atot3'F.5.8 has visible phenotype, suppressible | partially by sct5'eye

NOT suppressed by
Statement
Reference

ato1 has visible phenotype, non-suppressible by sct3'F.5.8/sct5'eye

ato1 has visible phenotype, non-suppressible by sct5'eye

ato1 has visible phenotype, non-suppressible by sct3'F.5.8

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

ato1/ato1090 has eye | heat sensitive phenotype, enhanceable by lilliAG5/lilli[+]

ato1/ato1090 has eye | heat sensitive phenotype, enhanceable by lilli[+]/lilliGD17

Suppressed by
Statement
Reference

ato1 has eye phenotype, suppressible | partially by amosRoi-1/amos[+]

ato1 has eye phenotype, suppressible | partially by scUAS.cCa/Scer\GAL47

ato1, atot5'eye has ommatidium phenotype, suppressible | partially by sct3'F.5.8

ato1, atot3'F.5.8 has ommatidium phenotype, suppressible | partially by sct5'eye

NOT suppressed by
Statement
Reference

ato1 has eye disc phenotype, non-suppressible by Mmus\Neurog1UAS.cQa/Scer\GAL47

ato1, atot3'F.5.8 has photoreceptor cell R8 phenotype, non-suppressible by sct5'eye

ato1 has photoreceptor cell R8 phenotype, non-suppressible by scUAS.cCa/Scer\GAL47

ato1 has ommatidium phenotype, non-suppressible by sct3'F.5.8/sct5'eye

ato1 has photoreceptor cell R8 phenotype, non-suppressible by sct3'F.5.8/sct5'eye

ato1 has ommatidium phenotype, non-suppressible by sct5'eye

ato1 has photoreceptor cell R8 phenotype, non-suppressible by sct5'eye

ato1 has ommatidium phenotype, non-suppressible by sct3'F.5.8

ato1 has photoreceptor cell R8 phenotype, non-suppressible by sct3'F.5.8

Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference

ato1/ato[+] is a non-enhancer of ommatidium phenotype of amosRoi-1

Suppressor of
Statement
Reference

ato1/Df(3R)p13 is a suppressor | partially of glial cell | ectopic & antennal disc phenotype of BacA\p35UAS.cHa, Scer\GAL4Dll-981

NOT Suppressor of
Other
Additional Comments
Genetic Interactions
Statement
Reference

A lilliGD17 heterozygous background dominantly enhances the ato1/ato1090 small, rough eye phenotype.

A lilliAG5 heterozygous background dominantly enhances the ato1/ato1090 small, rough eye phenotype.

Only 5% of abdominal segments contain a possible lch5 neuron in cato536 ; ato1 double homozygous embryos.

amos1 ; ato1 double mutant embryos show a complete lack of olfactory receptor neurons in the dorsal organ ganglion.

Expression of Egfr::toract.Scer\UAS under the control of Scer\GAL4GMR.PF in partially rescues the lack of cluster formation in the morphogenetic furrow of ato1 eye disc clones.

Expression of Egfr::toract.Scer\UAS under the control of Scer\GAL4GMR.PF partially rescues the lack of cluster formation in the morphogenetic furrow of ato1 eye disc clones.

ato1/Df(3R)p13 embryos lack C1 chordotonal organ precursor cells and have no larval oenocyte precursors. rhoScer\UAS.cdCa; Scer\GAL4en-e16E rescues the formation of larval oenocyte precursors in these embryos, but also causes additional induction and delamination of larval oenocyte precursors after the stage when this has ceased in wild-type embryos.

When BacA\p35Scer\UAS.cHa is driven by Scer\GAL4Dll-981 in the antennal disc of ato1/Df(3R)p13 mutants, only a partial suppression of the ectopic glial cell phenotype is seen. The fascicular organisation of the sensory afferents from the antenna is altered in mutants.

Expression of BacA\p35GMR.PH increase the size of ato1/Df(3R)p13 eyes by 25-30%. The increase in size is due to extra secondary pigment cells.

Expression of scScer\UAS.cCa under the control of Scer\GAL47 in ato1 flies rescues a small number of ommatidia. The eyes contain numerous interommatidial bristles in these flies.

When amos1 clones are made in ato1 animals the clone patch contains no sense organs except bristles.

The lack of oenocytes seen in ato1/Df(3R)p13 embryos is rescued by expression of rhoScer\UAS.cdCa under the control of Scer\GAL4en-e16E.

The eyes of amosRoi-1/+ ; ato1/ato1 flies can reach up to 1/3 of wild-type size. The ommatidial clusters appear disorganised and contain an abnormal number of photoreceptors, whose rhabdomeres are often elongated and misshapen. R8 cells appear to be present in most if not all ommatidia.

Combining Df(2L)GR4 (which removes the ASC: Achaete-scute Complex) and ato1 causes the loss of most cells in the embryonic peripheral nervous system (PNS) - only the two dorsal located md neurons remain. (which removes the ASC: Achaete-scute Complex)

ato1/+ ; da10/+ flies have significantly fewer sensilla coeloconica on the antenna than wild-type flies. lz3; ato1/ato1 double mutants show a complete absence of sensilla basiconica and coeloconica, as expected from loss of lz and ato functions respectively.

1 or 2 dorsal multiple dendritic neurons remain in each hemisegment in Df(1)sc-B57; ato1 embryos. amosScer\UAS.cHa rescues chordotonal neuron formation in odd segments in ato1 embryos when expressed under the control of Scer\GAL4h-1J3.

The addition of sct3'F.5.8 and sct5'eye to ato1 flies does not restore any boss-expressing R8 photoreceptors or ommatidia. The addition of sct3'F.5.8 and atot5'eye to ato1 flies does restore significant numbers of ommatidia and R8 receptors. The addition of atot3'F.5.8 and sct5'eye to ato1 flies does restore significant numbers of ommatidia but does not restore R8 receptors. This leads to an unusual arrangement of photoreceptors in the ommatidia. Many of these ommatidia contain fewer than eight photoreceptors, and most of the remaining photoreceptors resemble outer photoreceptors by their positions and the large size of their rhabdomeres. The expression of scScer\UAS.cCa when driven by Scer\GAL47 in ato1 flies does result in partial restoration of the compound eye. ommatidia contain only 2-5 photoreceptors, usually lacking the centrally located R8 photoreceptors with small rhabdomeres. Occasionally bristles that resemble macrochaetae are seen in various positions in the eye.

The addition of two copies of either or both sct3'F.5.8 and sct5'eye does not restore any boss-expressing R8 photoreceptors or ommatidia.

The addition of sct3'F.5.8 and atot5'eye to ato1 flies does restore significant numbers of ommatidia and R8 receptors, even though either transgene alone gives no rescue/suppression of this ato1 phenotype.

The addition of atot3'F.5.8 and sct5'eye to ato1 flies does restore significant numbers of ommatidia but does not restore R8 receptors, even though either transgene alone gives no rescue/suppression of this ato1 phenotype. This leads to an unusual arrangement of photoreceptors in the ommatidia. Many of these ommatidia contain fewer than eight photoreceptors, and most of the remaining photoreceptors resemble outer photoreceptors by their positions and the large size of their rhabdomeres.

The expression of scScer\UAS.cCa when driven by Scer\GAL47 in ato1 flies does result in partial restoration of the compound eye. Ommatidia contain only 2-5 photoreceptors, usually lacking the centrally located R8 photoreceptors with small rhabdomeres. Occasionally, bristles that resemble macrochaetae are seen in various positions in the eye.

da9; ato1 double heterozygotes exhibit reduced number of antennal coeloconic sensilla.

Df(1)sc10-1 ato1/Df(3R)p13 males do not show any decrease in the numbers of sensilla basiconica and trichodea.

Xenogenetic Interactions
Statement
Reference

Expression of Bmor\atoScer\UAS.cYb under the control of Scer\GAL4ato.eye suppresses the loss of eye phenotype found in ato1/Df(3R)p13 flies. However, ordered ommatidial packing is not restored as a number of supernumerary R8 cells are still present.

Expression of ato::Bmor\atoDmBm.Scer\UAS under the control of Scer\GAL4ato.eye in ato1/Df(3R)p13 results in mild suppression of the eye degeneration phenotype (less than upon expression of ato::Bmor\atoBmDm.Scer\UAS or ato, Bmor\ato single mutants).

Expression of ato::Bmor\atoDmBm.Scer\UAS under the control of Scer\GAL4ato.eye in ato1/Df(3R)p13 results in mild suppression of the eye degeneration phenotype (less than upon expression of ato, Bmor\ato single mutants).

Mmus\Neurog1Scer\UAS.cQa; Scer\GAL47 does not rescue eye disc phenotypes in ato1 homozygous animals.

Expression of Xlae\ath5aScer\UAS.cSa under the control of Scer\GAL47 restores the formation of R8 photoreceptor cells and numerous ommatidia in ato1 flies.

Expression of Mmus\Atoh7Scer\UAS.cSa under the control of Scer\GAL47 in ato1 flies rescues only a small number of ommatidia (less than 25 per eye) and none of these contain photoreceptor cells with clear R8 cell morphology. Interommatidial bristles are not produced in these flies.

Expression of Xlae\neuroDScer\UAS.cSa under the control of Scer\GAL47 restores the formation of R8 photoreceptor cells and numerous ommatidia in ato1 flies.

A single copy of P{UAS-Mmus\Atoh1.B} restores 3 of the 5 lateral chordotonal organs seen in wild-type, and 2 copies restores all of them, though occasionally a sixth organ is seen.

The chordotonal neuron phenotype is partially rescued by the expression of Mmus\Atoh1Scer\UAS.cBa under the control of Scer\GAL4hs.PB.

Complementation and Rescue Data
Partially rescued by
Not rescued by
Comments

Expression of atoScer\UAS.cYb under the control of Scer\GAL4ato.eye rescues the loss of eye phenotype found in ato1/Df(3R)p13 flies. However, ordered ommatidial packing is not restored as a number of supernumerary R8 cells are still present.

Expression of atoScer\UAS.cJa under the control of Scer\GAL47 restores the formation of R8 photoreceptor cells and numerous ommatidia in ato1 flies.

The lobular innervation pattern defect of ato1/Df(3R)p13 flies is rescued by atoScer\UAS.cJa expressed under the control of Scer\GAL4ato.3.6.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer

Separable from: a closely linked lethal mutation.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (84)