FB2024_03 , released June 25, 2024
Allele: Dmel\ago3
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General Information
Symbol
Dmel\ago3
Species
D. melanogaster
Name
FlyBase ID
FBal0126456
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description

Amino acid replacement: G1131E.

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

G4248277A

Amino acid change:

G1131E | ago-PA; G1131E | ago-PB; G1131E | ago-PC

Reported amino acid change:

G1131E

Comment:

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

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

ago3/agoΔ3-7 third instar larvae have tracheal defects, with the most prevalent phenotype being an approximate doubling of the number of cytoplasmic branches elaborated from multiple subtypes of terminal cells, including the lateral LH terminal cells.

ago3/ago1 embryos have breaks in their tracheal dorsal trunk.

ago3/+ embryos show a increased penetrance of tracheal phenotypes induced by 1% O[[2]] hypoxia treatment at stage 11, but not stage 15, compared to wild type.

ago1/ago3 transheterozygous mutants develop through all embryonic stages but fail to hatch as L1 larvae.

ago3/Df(3L)Exel9000 transheterozygous mutants develop through all embryonic stages but fail to hatch as L1 larvae.

ago1/ago3 mutant embryos exhibit defects in the developing trachea. The earliest of these are interruptions or 'breaks' in the continuity of the tracheal lumen. Approximately 70% of these mutants display breaks throughout the tracheal system and are prominent in the dorsal trunk, the lateral trunk, and between dorsal branches of opposing tracheal placodes. The dorsal branches and ganglionic branches also appear to show misrouting. The second prominent tracheal phenotype (occurring in 25% of embryos) is excess lumen convolution through the primary and secondary branches. Mutants have approximately the same number of nuclei per dorsal trunk segment, indicating that the primary effect of ago loss in the dorsal trunk is not on cell number, but on fusion cell migration and fusion.

In ago3 homozygous embryos, 5% of hemisegments have two RP2 sibs and one RP2 neuron, while others have two RP2 neurons and one sib, rather than the one cell of each type seen in each segment in wild-type embryos. In ago3/Df(3L)GN50 embryos this increases to 7%.

Adult eyes mosaic for ago3 are composed mostly of mutant tissue, exhibiting a proliferative advantage over their wild-type twin-spots. Within mutant clones, most ommatidial clusters lack the wild-type complement of photoreceptor cells, and the distance between adjacent photoreceptor clusters is increased. The large interommatidial spaces in these clones contain excess cells compared to wild-type (from 12 to about 20 per photoreceptor cluster). There is no decrease in the extent of cell death in these clones. When homozygous mutant clones are made in the wing disc, a smaller fraction of cells (21.4%) is found in G1 compared to wild-type cells (36.%). The proportion of cells in S phase is increased. In pupal eye discs cell cycling continues after the corresponding cells in wild-type tissues have exited the cell cycle.

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

ago[+]/ago3 is a suppressor of visible phenotype of CycEJP

Other
Phenotype Manifest In
Enhanced by
Suppressed by
Statement
Reference

ago3, slmb00295 has glial cell | embryonic stage phenotype, suppressible by gcmN7-4/gcm[+]

ago3, slmb00295 has glial cell | embryonic stage phenotype, suppressible by gcm26

ago3/ago1 has tracheal primordium phenotype, suppressible by trh10512/trh[+]

ago3/ago1 has tracheal fusion cell phenotype, suppressible by trh10512/trh[+]

ago3/ago1 has tracheal lumen phenotype, suppressible by btl[+]/btldev1

ago3/ago1 has tracheal primordium phenotype, suppressible by btl[+]/btldev1

ago3/ago1 has tracheal fusion cell phenotype, suppressible by btl[+]/btldev1

ago3/ago1 has tracheal lumen phenotype, suppressible by trh10512/trh[+]

Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

ago[+]/ago3 is a suppressor of eye phenotype of CycEJP

Other
Additional Comments
Genetic Interactions
Statement
Reference

simaKG07607 dominantly delays the lethal phase of agoΔ3-7/ago3 transheterozygotes.

simaKG07607 dominantly suppresses the increase in number of terminal branches per lateral LH cell seen in ago3/agoΔ3-7 larvae.

slmb00295, ago3 double mutant embryos display a disrupted glial pattern compared to single mutant or control embryos. An increase in repo-positive glial cell number is observed. An increase in cell proliferation is observed, and no increase in cell death is seen.

Expression of slmbαTub84B.T:Hsap\MYC in slmb00295, ago3 double mutant embryos significantly suppresses the increased number of glial cells observed in the slmb00295, ago3 mutant embryos.

slmb00295, ago3, gcmN7-4 triple mutants results in the absence of almost all glia, as observed in gcmN7-4 single mutants. One copy of gcmN7-4 suppresses the increased glial cell number phenotype observed in slmb00295, ago3 double mutants.

gcm26 suppresses the increased glial cell number phenotype observed in slmb00295, ago3 double mutants.

ago3/+ enhances the tracheal phenotypes seen when Scer\GAL4btl.PS mediates expression of relatively weaker VhldsRNA.Scer\UAS lines, particularly enhancing the penetrance of migration defects.

Embryos trans-heterozygous for ago3 and Df(2R)Exel6060 (that uncovers Vhl) show an elevated frequency of tracheal fusion and migration defects compared to either lesion alone.

Df(2R)Exel6060 (that uncovers Vhl) dominantly enhances the number of dorsal trunk breaks per affected ago3/ago1 embryo.

A trh10512 heterozygous background dominantly suppresses the tracheal phenotypes found in ago1/ago3 mutants.

A btldev1 heterozygous background dominantly suppresses the tracheal phenotypes found in ago1/ago3 mutants.

A awdj2A4 heterozygous background strongly enhances both the penetrance (from 46% of embryos to greater than 80% of embryos) of the ago1/ago3 mutant dorsal trunk phenotype and its expressivity among affected embryos. These embryos also show a much more severe disruption of the entire tracheal system compared to ago1/ago3 mutants.

ago3 does not protect Df(1)su(s)R194/+ clones in the eye; Df(1)su(s)R194/+ ; ago3 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, ago3 does not prevent apoptosis of Df(1)su(s)R194/+ cells in the wing.

The expression of BacA\p35GMR.PH in BacA\p35GMR.PH somatic clones in the eye, results in an increase in the number of interommatidial cells (from about 20 to about 40 per photoreceptor cluster).

Xenogenetic Interactions
Statement
Reference

The expression of BacA\p35GMR.PH in ago3 somatic clones in the eye, results in an increase in the number of interommatidial cells (from about 20 to about 40 per photoreceptor cluster).

Complementation and Rescue Data
Comments

Expression of agoScer\UAS.cMa in the developing tracheal system under the control of Scer\GAL4btl.PS in an ago1/ago3 mutant background significantly reduces the frequency of dorsal trunk breaks, along with other tracheal phenotypes.

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Wild-type
Stocks (0)
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External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
References (14)