In many animals, the bipolar spindle of the first zygotic division is established after the contribution of centrioles by the sperm at fertilization. To avoid the formation of a multipolar spindle in the zygote, centrosomes are eliminated during oogenesis in most organisms, although the mechanism of this selective elimination is poorly understood. We show that cki-2, a Caenorhabditis elegans cyclin-dependent kinase (Cdk) inhibitor, is required for their appropriate elimination during oogenesis. In the absence of cki-2, embryos have supernumerary centrosomes and form multipolar spindles that result in severe aneuploidy after anaphase of the first division. Moreover, we demonstrate that this defect can be suppressed by reducing cyclin E or Cdk2 levels. This implies that the proper regulation of a cyclin E–Cdk complex by cki-2 is required for the elimination of the centrosome that occurs before or during oogenesis to ensure the assembly of a bipolar spindle in the C. elegans zygote.
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11 September 2006
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September 05 2006
Cell cycle regulators control centrosome elimination during oogenesis in Caenorhabditis elegans
Dae Young Kim,
Dae Young Kim
Department of Biology, McGill University, Montreal, Quebec H3A 1B1, Canada
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Richard Roy
Richard Roy
Department of Biology, McGill University, Montreal, Quebec H3A 1B1, Canada
Search for other works by this author on:
Dae Young Kim
Department of Biology, McGill University, Montreal, Quebec H3A 1B1, Canada
Richard Roy
Department of Biology, McGill University, Montreal, Quebec H3A 1B1, Canada
Correspondence to Richard Roy: [email protected]
Abbreviations used in this paper: CKI, Cdk inhibitor; dsRNA, double-stranded RNA.
Received:
December 29 2005
Accepted:
August 07 2006
Online ISSN: 1540-8140
Print ISSN: 0021-9525
The Rockefeller University Press
2006
J Cell Biol (2006) 174 (6): 751–757.
Article history
Received:
December 29 2005
Accepted:
August 07 2006
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Citation
Dae Young Kim, Richard Roy; Cell cycle regulators control centrosome elimination during oogenesis in Caenorhabditis elegans . J Cell Biol 11 September 2006; 174 (6): 751–757. doi: https://doi.org/10.1083/jcb.200512160
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