Letter abstract


Nature Cell Biology 6, 777 - 783 (2004)
Published online: 11 July 2004 | doi:10.1038/ncb1154

The CDC-14 phosphatase controls developmental cell-cycle arrest in C. elegans

R. Mako Saito1, Audrey Perreault1, Bethan Peach1, John S. Satterlee1 & Sander van den Heuvel1

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Temporal control of cell division is critical for proper animal development. To identify mechanisms involved in developmental arrest of cell division, we screened for cell-cycle mutants that disrupt the reproducible pattern of somatic divisions in the nematode C. elegans. Here, we show that the cdc-14 phosphatase is required for the quiescent state of specific precursor cells. Whereas budding yeast Cdc14p is essential for mitotic exit, inactivation of C. elegans cdc-14 resulted in extra divisions in multiple lineages, with no apparent defects in mitosis or cell-fate determination. CDC-14 fused to the green fluorescent protein (GFP–CDC-14) localized dynamically and accumulated in the cytoplasm during G1 phase. Genetic interaction and transgene expression studies suggest that cdc-14 functions upstream of the cki-1 Cip/Kip inhibitor to promote accumulation of CKI-1 in the nucleus. Our data support a model in which CDC-14 promotes a hypophosphorylated and stable form of CKI-1 required for developmentally programmed cell-cycle arrest.

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  1. Massachusetts General Hospital Cancer Center and Harvard Medical School, Building 149, 13th Street, Charlestown, Massachusetts 02129, USA.

Correspondence to: Sander van den Heuvel1 e-mail: heuvel@helix.mgh.harvard.edu



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