FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\mago1
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General Information
Symbol
Dmel\mago1
Species
D. melanogaster
Name
FlyBase ID
FBal0032138
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

Amino acid replacement: G19R.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Nucleotide change:

G21128748A

Amino acid change:

G19R | mago-PA

Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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
Detailed Description
Statement
Reference

Ooplasmic streaming is normal at stage 9 and stage 10b in mago1/Df(2R)F36 oocytes.

The nucleus fails to migrate to the anterior of the oocyte in approximately 30% of the egg chambers of mago1/Df(2R)F36 females at 18oC. The penetrance of this phenotype is less than 3% at 25oC. The nucleus also fails to migrate to the anterior of the oocyte in some of the egg chambers of mago1/mago1 and mago1/mago2 females. Stage 9 mago1/Df(2R)F36 egg chambers have an abnormal distribution of microtubules at 18oC, with high levels of microtubules at both poles of the oocyte and lower levels in the centre. Microtubule organisation appears more normal in later stage egg chambers at 18oC, although a small posterior focus of microtubules often persists until stage 10-11. Microtubule organisation appears more normal in mago1/Df(2R)F36 egg chambers at 25oC, although a small focus of microtubules is seen at the posterior pole during stages 8-9. Approximately 30% of eggs laid by mago1/Df(2R)F36 females are symmetrical along the dorsal-ventral axis. These eggs are completely ventralised at the anterior end; they lack dorsal appendages, the operculum develops as a symmetric ring around the micropyle and the micropyle points anteriorly rather than dorsally. The egg shell is more pointed at the posterior pole than normal, and the posterior aeropyle is larger and more symmetric than wild-type.

Approximately 1% of eggs derived from hemizygous females raised at 25oC are ventralised. Approximately 38% of eggs derived from hemizygous females shifted from 25oC to 17oC are ventralised. The dorsal appendages are missing in these ventralised eggs and the micropyle canal is defective, although the aeropyle appears normal. Approximately 1% of eggs derived from hemizygous females raised at 25oC contain a mislocalised oocyte nucleus. Approximately 36% of eggs derived from hemizygous females shifted from 25oC to 17oC contain a mislocalised oocyte nucleus. Homozygous female germline clones also give rise to egg chambers containing mislocalised oocyte nuclei and ventralised eggs. The polarisation of the microtubule cytoskeleton is abnormal in hemizygous egg chambers shifted from 25oC to 17oC.

Prevents the posterior accumulation of G-iα65A protein.

Offspring fail to make pole cells. Shows temperature sensitive defects in abdominal segmentation and embryonic body plan.

When mutant females are raised at 25oC some of the resulting embryos have double abdomens. At 17oC the females produce embryos displaying abdominal defects typical of the posterior group, with no incidence of head defects or double abdomens.

Grandchildless-like phenotype. Eggs from homozygous females have no apparent posterior determinants in the posterior pole. At 17oC the inviable embryos lack abdominal segments, at 25oC a novel gene product is produced that is capable of inducing the formation of symmetrical double abdomen embryos (behave as recessive antimorphs). The temperature sensitive period is during oogenetic stages 7--14.

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

mago1 has sterile phenotype, suppressible by Cele\mag-1mago.PN

Enhancer of
Statement
Reference

mago1/mago[+] is an enhancer of visible phenotype of rl1

mago1/mago[+] is an enhancer of visible phenotype of cswlf

Suppressor of
Statement
Reference

mago1/mago[+] is a suppressor of visible | dominant phenotype of EgfrE1

mago1/mago[+] is a suppressor of visible phenotype of Ras85DV12.sev

Other
Phenotype Manifest In
Suppressed by
Enhancer of
Statement
Reference

mago1/mago[+] is an enhancer of eye phenotype of rl1

mago1/mago[+] is an enhancer of wing vein phenotype of rl1

mago1/mago[+] is an enhancer of wing vein phenotype of cswlf

Suppressor of
Statement
Reference

mago1/mago[+] is a suppressor of wing vein | ectopic phenotype of EgfrE1

mago1/mago[+] is a suppressor of eye phenotype of Ras85DV12.sev

Other
Additional Comments
Genetic Interactions
Statement
Reference

Embryos derived from mago1/Df(3R)p-XT103 mutants exhibit abdominal and head defects (in up to 35% of embryos). The presence of one copy of oskt.WT partially suppresses these defects while the presence of one copy of oskS244A.S248A exacerbates these defects and increases the number of bicaudal embryos.

mago1 dominantly suppresses the rough eye phenotype caused by Ras85DV12.sev.

mago1 dominantly enhances the loss of wing vein phenotype seen in cswlf/Y flies.

The extra wing vein phenotype seen in EgfrE1/+ flies is dominantly suppressed by mago1.

The loss of wing veins and rough eye phenotype seen in rl1 homozygotes is dominantly enhanced by mago1.

A mago1 heterozygous background enhances eye degeneration found in Scer\GAL4GMR.PF>cln3Scer\UAS.T:Avic\GFP-YFP.Venus flies.

Wing phenotypes found with overexpression of cln3Scer\UAS.cTa with Scer\GAL4en-e16E are enhanced in a mago1 heterozygous background.

Embryos that express miraΔ103.αTub67C.T:Avic\GFP-m6 in a mago1/Df(2R)F36 background have no posterior abdomen and have an anterior abdomen of reversed polarity.

Xenogenetic Interactions
Statement
Reference

A single copy of Cele\mag-1mago.PN is sufficient to rescue the axis defects and sterility caused by mago1.

Complementation and Rescue Data
Comments

Defects in axis formation and germ-plasm assembly caused by mago1 are rescued by mago+t2.2.T:Hsap\MYC and also by mago+t2.2.T:Avic\GFP.

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

Although tud protein is present in mutant embryo extracts, its localization in the embryo is altered.

Shows interallelic complementation for zygotic lethality with magoE19A and magoWE7.

Germ line clonal analysis indicates that mago function is required in the germ line.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
References (26)