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General Information
Symbol
Dmel\AGO2414
Species
D. melanogaster
Name
FlyBase ID
FBal0162855
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
ago-2414
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
Imprecise excision of the P{EP}AGO2EP3417 insertion has created a partial deletion of the AGO2 gene. Exon 2 and most of intron 2 have been removed.
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
AGO2414 homozygotes show a significant increase in viral load in the head upon infection with SINV, but not with ZIKV, as compared to infected controls.
The survival rate of DIP1EY02625 mutants after DCV infection is 30% compared to controls. Median survival is 5-6 days.
Compared with wild-type, AGO2414 mutant flies show increased sensitivity to Invertebrate Iridescent Virus type 6 (IIV-6) infection. The mutant flies also contain more viral DNA than do wild-type controls.
AGO2414 homozygotes are short lived compared to controls. 2-4 day old AGO2414/AGO251B transheterozygous adults show a mild defect in 24 hour memory after spaced training compared to wild type. This defect is markedly worse in 20 day old adults.
AGO2414 mutant flies are more susceptible to non-virulent Flock house virus (FHV) mutant infection than wild-type. The FHV mutant that lacks viral protein FHV\B2, a known RNAi suppressor, is not pathogenic in wild-type flies, but AGO2414 mutants show decreased survival after infection. Unlike the case in wild-type flies, the FHV FHV\B2 mutant replicates to high levels in AGO2414 mutants.
More than 60% of cells in anaphase mutant wing discs contain lagging chromosomes.
AGO2414 mutants display a reduction in dsRNA processing and a subsequent ~86% reduction in siRNA levels.
AGO2414 mutant flies show severely compromised survival when infected with vesicular stomatitis virus, and die within 12 days of infection. Viral titres are significantly higher compared to controls.
AGO2414/+ significantly suppresses the position effect variegation of the Sb1 allele that is seen in the T(2;3)SbV chromosome.
Homozygous projection neuron (PN) clones show normal dendrite and axon targeting in adPN clones and in DL1 single cell projection neuron clones.
Flock house virus (FHV) viral RNA accumulates at greater levels in AGO2414 embryos than in wild-type embryos.
Mutant flies are hypersensitive to infection with either Drosophila C virus (DCV) or Cricket Paralysis virus (CrPV); the median survival after inoculation with 350 TCID50 of DCV or CrPV is reduced compared to controls, and the 50% lethal dose of virus is much lower than for control flies. Even at early time points after inoculation with DCV, viral titers in mutant flies are 1000-fold higher than in controls.
The distance from one nucleus to the next is variable in AGO2414 presyncytial and syncytial embryos compared to regular in wild-type, with nuclei found clustered in some regions of the embryo while they are absent in other regions. Many AGO2414 nuclei fail to migrate to the surface, while others appear to reach the surface but then fall back into the interior of the embryo, consequently the nuclear distribution at the surface is quite irregular. In some regions there is a high concentration of nuclei, often linked together in 'strings' of two, three, or four incompletely separated nuclei, while in other regions there are very few. There is also evidence that some nuclei may have more than the normal complement of DNA while others may be missing DNA. Defects in chromosomal migration are also evident prior to nuclear migration in AGO2414 mutant embryos. Consistent with the requirement for AGO2 in the proper execution of the mitotic cycle, anomalous anaphase figures with incompletely condensed and irregularly positioned chromosomes are observed in the AGO2414 mutant. Nearly 10-15% of AGO2414 mutant embryos do not hatch. A variety of anomalies are evident in AGO2414 embryos. In the early cleavage stage embryo, nuclei can be fragmented and can appear to have incompletely separated but still enter mitosis. In older embryos, asynchrony is occasionally observed in incompletely separated nuclei. During metaphase in AGO2414 embryos, nuclei appear to undergo a normal mitosis in approximately half of the cases. In the other half, defects such as 'orphan' centrosomes pairs are observed. While the duplicated centrosomes occasionally remain in close proximity, most appear to migrate to opposite poles. These 'orphan' centrosome pairs are not associated with a mitotic spindle apparatus or with mitotic chromosomes, nor does there appear to be any nearby interphase nucleus. While other centrosome pairs appear to properly nucleate the mitotic spindle apparatus, the spindles are abnormally short and do not extend to the chromosomes or make connections with the centromeres. The chromosomes often appear to be displaced from their normal position in the center of the metaphase plate. In other cases there are DNA bridges that extend between two adjacent mitotic figures. There are also 'mitotic spindle' bridges that connect two different mitotic figures. In half of AGO2414 embryos the cytoskeleton, normally a regular lattice, is replaced by a broken network with irregularly shaped contractile rings that vary in thickness from one part of the ring to the next. Some of these scra-labelled rings appear to contain multiple nuclei, while other rings have neither nuclei nor DNA. The total number of pole cells is much reduced in AGO2414 embryos (8, compared to 20 per embryo in wild-type). These pole cells are often not positioned correctly at the very posterior or are separated from each other by somatic cells. There is also a great deal of variability in the number of pole cells in AGO2414 mutants compared to wild-type. While some AGO2414 embryos have only two or three pole cells, there are a few that have near wild-type numbers. This reduction in the number of pole cells can be traced back to nuclear cycle 8-9 when migrating nuclei first enter the posterior pole plasm. Several nuclear cycle 8-9 AGO2414 embryos have fewer pole buds than wild-type.
Mutant animals exhibit a resistance to RNA interference from injected dsRNAs.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Suppressor of
NOT Suppressor of
Statement
Reference
AGO2414 is a non-suppressor of eye phenotype of wIR.GMR
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference
The mortality exhibited by flamA, ctA double homozygotes is suppressed by either AGO2414 heterozygosity (partial suppression) or AGO2414, AGO3t2 double heterozygosity (full suppression).
The eyes of wdsRNA.GMR transgenic female flies homozygous for AGO2414 are similar to that of wild-type.
The survival of roX1ex33A Df(1)roX2Δ adult males is reduced if they are also heterozygous for AGO2414. AGO2414/+ partially suppresses the delay in peak eclosion which is seen in females expressing msl-2Hsp83.PK. roX1ex40A Df(1)roX2Δ ; AGO2414/AGO2414 males show only 8% survival.
The eye colour of wdsRNA.Scer\UAS.cKa, Scer\GAL4GMR.PF flies reverts to red in a AGO2414 background.
AGO2414 mutant flies carrying two copies of wIR.GMR fail to silence the w gene and exhibit red eyes.
Double mutant AGO1k08121 AFO2414 projection neuron (PN) clones show normal glomerular target selection in adPN clones and in DL1 single cell projection neuron clones.
Xenogenetic Interactions
Statement
Reference
An AGO2414 homozygous background dramatically mitigates the toxicity found upon co-expression of Disc\RFP(CTG)200.Scer\UAS and Disc\RFPCAG250.DsRed2.Scer\UAS in the developing eye, under the control of Scer\GAL4GMR.PF.
Co-expression of both Zzzz\CCG90.Scer\UAS.T:Avic\GFP-EGFP and Zzzz\CGG90.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4GMR.PU suppresses the disorganised external eye phenotype and photoreceptor cell degeneration which is seen when either construct is expressed singly under the control of Scer\GAL4GMR.PU. This mutual suppression by Zzzz\CCG90.Scer\UAS.T:Avic\GFP-EGFP and Zzzz\CGG90.Scer\UAS.T:Avic\GFP-EGFP does not occur if they are co-expressed under the control of Scer\GAL4GMR.PU in a AGO2414 homozygous background - in this case, the flies show pupal lethality and have a more severe eye phenotype than that seen when either construct is expressed singly.
Complementation and Rescue Data
Fails to complement
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (56)