wash^Δ185/+ RpII140^wimp/+ trans-heterozygotes exhibit disrupted actin organization at outer ring canals in stage 7-9 egg chambers, premature ooplasmic streaming in stage 7 oocytes and disrupted cortical actin organization in stage 7-9 oocytes when compared to controls.

-actin projections in the posterior region of Rho1^72F/+ ; RpII140^wimp/+ stage 10b oocytes are reduced compared to wild-type oocytes.

Stage 7 oocytes show premature cytoplasmic streaming in wash^Δ185/+ ; RpII140^wimp/+ females. The yolk granules show speeds of movement that are almost twice that seen in wild type and the movements are concerted and coordinated, in contrast to the uncoordinated, saltatory movements seen in wild-type oocytes at this stage. The normal gradient of microtubule organisation that is seen in wild-type oocytes at this stage is lost in the mutant oocytes. The oocyte nucleus is mislocalised in the mutant oocyte by stage 7 and contains to be mislocalised during later stages. The mutant stage 7 oocytes have a disrupted and discontinuous band of cortical actin.

wash^Δ185/+ ; RpII140^wimp/+ egg chambers show a loss of nurse cell integrity at stage 10a and incomplete stress fiber formation during during nurse cell dumping (stages 10b-11) compared to wild type. The actin network around the ring canals is abnormally expanded during nurse cell dumping in the mutant egg chambers. Inner ring canal formation appears to be unaffected, although ring canals separated from the nurse cell membrane can be found floating within the oocyte.

wash^Δ185/+ ; RpII140^wimp/+ Arpc1^Q25st egg chambers show a loss of nurse cell integrity at stage 10a and incomplete stress fiber formation during during nurse cell dumping (stages 10b-11) compared to wild type. The actin network around the ring canals is abnormal by stage 10b.

Stage 8 oocytes from Rho1^1B; RpII140^wimp mothers exhibit premature ooplasmic streaming and subcortical arrays of microtubules. Stable microtubules are restricted to the cortex, as in wild-type oocytes, but differ in the lack of reduction of microtubules at the posterior pole.

Embryos derived from Sir2^05327a/+ ; RpII140^wimp/+ females (mated to wild-type males) die and show anterior-posterior patterning defects, including loss of segments and pairwise denticle band fusions. Embryos derived from Sir2^ex10/+ ; RpII140^wimp/+ females (mated to wild-type males) die and show anterior-posterior patterning defects, including loss of segments and pairwise denticle band fusions.

Rho1^rev220/+; +/RpII140^wimp females show disrupted actin cytoskeletal structure in the egg chambers, particularly in the outer ring canals and oocyte cortex. The inner ring canals appear relatively normal.

Embryos derived from mothers transheterozygous for RpII140^wimp and CtBP⁰³⁴⁶³ die and cuticle preparations of the embryos show segmentation defects ranging from pair-wise fusion of adjacent denticle belts to more widespread denticle fusions.

Ovaries from ct^C145/+ ; RpII140^wimp/+ females contain egg chambers with an abnormal number of germline cells and show cyst encapsulation defects. No multinucleate cells are seen in the egg chambers. Ovaries from ct^L188/+ ; RpII140^wimp/+ females show no abnormal phenotype.