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.

(Liu et al., 2018)

The survival rate of DIP1^EY02625 mutants after DCV infection is 30% compared to controls. Median survival is 5-6 days.

(Zhang et al., 2015)

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.

(Kemp et al., 2013)

AGO2⁴¹⁴ homozygotes are short lived compared to controls. 2-4 day old AGO2⁴¹⁴/AGO2^51B 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.

(Li et al., 2013)

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.

(Han et al., 2011)

More than 60% of cells in anaphase mutant wing discs contain lagging chromosomes.

(Pek and Kai, 2011)

AGO2⁴¹⁴ mutants display a reduction in dsRNA processing and a subsequent ~86% reduction in siRNA levels.

(Marques et al., 2010)

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.

(Mueller et al., 2010)

AGO2⁴¹⁴/+ significantly suppresses the position effect variegation of the Sb¹ allele that is seen in the T(2;3)Sb^V chromosome.

(Fagegaltier et al., 2009)

Homozygous projection neuron (PN) clones show normal dendrite and axon targeting in adPN clones and in DL1 single cell projection neuron clones.

(Berdnik et al., 2008)

Flock house virus (FHV) viral RNA accumulates at greater levels in AGO2⁴¹⁴ embryos than in wild-type embryos.

(Wang et al., 2006)

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.

(van Rij et al., 2006)

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.

(Deshpande et al., 2005)

Mutant animals exhibit a resistance to RNA interference from injected dsRNAs.

(Okamura et al., 2004)

AGO2⁴¹⁴/AGO2[+] is a suppressor | partially of partially lethal - majority live phenotype of ct^A, lncRNA:flam^A

(Guida et al., 2016)

AGO3[+], AGO2⁴¹⁴, AGO3^t2, AGO2[+] is a suppressor of partially lethal - majority live phenotype of ct^A, lncRNA:flam^A

(Guida et al., 2016)

AGO2⁴¹⁴ is a suppressor of visible phenotype of w^dsRNA.GMR/w^dsRNA.GMR

(Fukunaga et al., 2012)

AGO2⁴¹⁴/AGO2[+] is a suppressor | partially of developmental rate defective | female phenotype of msl-2^Hsp83.PK

(Menon and Meller, 2012)

AGO2⁴¹⁴ is a suppressor of eye color defective phenotype of Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, w^{dsRNA.UAS.cKa}

(Sanders and Smith, 2011)

AGO2⁴¹⁴, Df(1)roX2Δ, lncRNA:roX1^ex40A has partially lethal - majority die | male phenotype

(Menon and Meller, 2012)

AGO2⁴¹⁴, Scer\GAL4^GMR.PU, Zzzz\CCG^90.UAS.EGFP, Zzzz\CGG^90.UAS.EGFP/Zzzz\CGG^{90.Scer\UAS.T:Avic\GFP-EGFP} has lethal | pupal stage phenotype

(Sofola et al., 2007)

AGO2⁴¹⁴, w^+mW.hs has eye color defective phenotype

(Deshpande et al., 2005)

AGO2⁴¹⁴, w[+]/w^+mW.hs has eye color defective phenotype

(Deshpande et al., 2005)

AGO2⁴¹⁴ is a suppressor of eye phenotype of w^dsRNA.GMR/w^dsRNA.GMR

(Fukunaga et al., 2012)

AGO2⁴¹⁴ is a suppressor of eye phenotype of Disc\RFP^{(CTG)200.Scer\UAS}/Zzzz\CTG^{200.UAS.DsRed2}, Disc\RFP^{CAG250.DsRed2.Scer\UAS}/Zzzz\CAG^{250.UAS.DsRed2}, Scer\GAL4^GMR.PF

(Yu et al., 2011)

AGO2⁴¹⁴ is a suppressor of retina phenotype of Disc\RFP^{(CTG)200.Scer\UAS}/Zzzz\CTG^{200.UAS.DsRed2}, Disc\RFP^{CAG250.DsRed2.Scer\UAS}/Zzzz\CAG^{250.UAS.DsRed2}, Scer\GAL4^GMR.PF

(Yu et al., 2011)

AGO2⁴¹⁴, w^+mW.hs has eye phenotype

(Deshpande et al., 2005)

AGO2⁴¹⁴, w[+]/w^+mW.hs has eye phenotype

(Deshpande et al., 2005)