Expression of tocdsRNA.Scer\UAS under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16 in female flies has a dose-dependent effect on their offspring: one copy of either transgene results in lethality of ~36% of offspring, two copies of one transgene and one copy of the other results in 90% embryonic lethality, and two copies of both transgene results in complete embryonic lethality. The lethality of embryos from mothers with one copy of each transgene is increased when mothers are heterozygous for tocP or tocPR3. Expression of two copies of tocdsRNA.Scer\UAS, under the control of two copies of Scer\GAL4mat.αTub67C.T:Hsim\VP16, in females causes their offspring to experience an early arrest of syncytial mitoses in a pseudometaphase state. These arrested embryos have short mitotic spindles with broad poles and no attached centrosomes. Expression of one copy of tocdsRNA.Scer\UAS, under the control of one copy of Scer\GAL4mat.αTub67C.T:Hsim\VP16, in females affects the syncytial mitoses of their offspring. The first few mitoses proceed as wild type, then defects start to occur. At metaphase, spindles are shorter than in wild-type embryos and there is no significant elongation of spindles in later mitotic stages. During anaphase, spindle microtubules disappear, resulting in the absence of the central spindle and the formation of elongated nuclei extending from one centrosome to the other at the end of mitosis. Chromosome segregation is not fully completed, as can be observed by the formation of an ovoid mass of chromosomes at the end of the mitoses. Interpolar and kinetochore microtubules are absent throughout the aberrant mitoses. Astral microtubules are not affected.
Transfected into flies to study the phenotypic consequences of dsRNA interference (RNAi) of the toc gene.