In AGO251B mutants the RNA interference function is lost and so adult flies expressing wdsRNA.GMR retain the red eye color.
Embryos derived from AGO251B mothers are largely morphologically normal and show no defects in the transport of lipid droplets. A minor fraction exhibit defects during syncytial cleavages and do not develop beyond that stage.
Nearly 40% of AGO251B mutant embryos do not hatch. The total number of pole cells observed in AGO251B mutants is reduced compared to wild-type (12 compared to 20 per embryo). 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.
AGO251B/AGO251B is a suppressor of increased cell death phenotype of Diap1RNAi.UAS, Scer\GAL4GMR.PF
AGO251B/AGO251B is a suppressor of eye phenotype of Diap1RNAi.UAS, Scer\GAL4GMR.PF
In flies homozygous for AGO251B, the Scer\GAL4GMR.PF>thdsRNA.Scer\UAS small eye phenotype is completely suppressed.
Embryos from AGO1k08121; AGO251B double mutant parents exhibit segment polarity defects that are not seen in either single mutant.
AGO251B is rescued by AGO2+t10.15
The loss of RNA interference functionality characteristic for AGO251B mutants and manifested by their retaining red eye color upon expression of wdsRNA.GMR is rescued by combination with either AGO2+t10.15 or AGO2m2 and results in very light variegated eye pigmentation, whereas combination with AGO2m1 leads to only partial rescue and light red eye color.