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- Publisher
- Springer Journals
- Copyright
- Copyright © 2004 by Nature Publishing Group
- Subject
- Life Sciences; Life Sciences, general; Cell Biology; Cancer Research; Developmental Biology; Stem Cells
- ISSN
- 1465-7392
- eISSN
- 1476-4679
- DOI
- 10.1038/ncb1154
- Publisher site
- See Article on Publisher Site
Abstract
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.
Journal
Nature Cell Biology – Springer Journals
Published: Jul 11, 2004