A one-cell embryo with too little cki-2 forms a tetrapolar spindle (red) due to extra centrosomes (green).
In most organisms, centrosomes are removed from the developing egg to prevent the fertilized zygote from inheriting redundant sets from both the egg and the sperm. But too many of these microtubule organizers is just what Kim and Roy found upon reducing levels of cki-2, a negative regulator of cell cycle progression.
The affected zygotes arrested at the one-cell stage with an extra pair of centrosomes and often multiple nuclei. Working backwards from there, the group found that the extra centrosomes came from the egg.
Like the paternal centrosomes, the extra set nucleated its own spindle microtubules and thus created havoc during cell division. The problem was corrected by reducing levels of CDK2, a known cki-2 target. The authors theorize that activation of cki-2 at oogenesis might destabilize centrosomes by blocking the phosphorylation of centriolar proteins, many of which have consensus CDK2 phophorylation sites.
These maternal centrosomes are not exactly like their sperm counterparts, however. In the zygote, the egg centrosomes sometimes detached from the normal position on the nuclear envelope and floated around in the cytoplasm. Despite their random location, maternal centrosomes did not interfere with zygote polarity, which is established by the sperm set. This distinction suggests that the male centriole might enter the oocyte with a unique set of associated proteins. Alternatively, specific centriole interactions with the cortex might be necessary.
Elimination of the maternal centrosomes, which occurs in most organisms, favors sexual reproduction, as only the egg supplies the pericentriolar material and only the sperm provides the centrioles. If the egg harbored both, it might make its own mature spindle-organizing centrosome and be able to develop parthogenetically. 
