Recently, systematic screens of C. elegans using RNAi have identified many genes required for early embryonic development. When the expression of one such identified gene,Y18D10A.17, is blocked using RNAi, defects in cytokinesis are observed in the embryo (Zipperlen et al., 2001 EMBO J 20:3984). Suppression of this gene, named
car-1 (cytokinesis, apoptosis, and RNA), caused embryos to fail at the time of scission, when the persisting intercellular canal is normally broken and the membranes re-seal. The late accumulation of membrane to the furrow tip seen in wild-type embryos did not occur in
car-1(RNAi) embryos. Observations of microtubule organization in these embryos revealed that mitotic spindles underwent exaggerated rocking at the one cell stage and had no visible microtubules in the spindle midzone at anaphase. Furthermore, the midzone component, ZEN-4, is mislocalized in
car-1(RNAi) embryos, which also exhibit chromosome segregation defects as well as a disruption in the proper organization of the endoplasmic reticulum. A GFP::CAR-1 construct localized to p-granules and to smaller, temporally regulated cytoplasmic puncta in all cells. These smaller puncta also include the worm homolog of the RNA decapping protein DCP1, suggesting that CAR-1 plays some role in RNA processing.
car-1 is a conserved gene that, at least in C. elegans embryos, provides an interesting link between RNA processing and cytokinesis.