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Updated: Aug 23, 2026

Cell Cycle Analysis in the C. elegans Germline with the Thymidine Analog EdU
Published on: October 22, 2018
The CDC-14 phosphatase controls developmental cell-cycle arrest in C. elegans
R Mako Saito1, Audrey Perreault, Bethan Peach
1Massachusetts General Hospital Cancer Center and Harvard Medical School, Building 149, 13th Street, Charlestown, Massachusetts 02129, USA.
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.
Insights
The cdc-14 phosphatase in C. elegans controls cell division timing, promoting developmental cell-cycle arrest. It ensures precursor cells enter a quiescent state by stabilizing the CKI-1 inhibitor.
Area of Science:
- Developmental Biology
- Cell Cycle Regulation
- Genetics
Background:
- Precise temporal control of cell division is essential for animal development.
- Understanding mechanisms of developmental cell-cycle arrest is crucial.
Purpose of the Study:
- To identify genes regulating developmental cell-cycle arrest in C. elegans.
- To elucidate the role of the cdc-14 phosphatase in cell division timing.
Main Methods:
- Screening for cell-cycle mutants in C. elegans.
- Analyzing the function of cdc-14 phosphatase through genetic interactions and GFP tagging.
- Investigating the interaction between cdc-14 and the cki-1 inhibitor.
Main Results:
- cdc-14 is required for the quiescent state of specific precursor cells.
- cdc-14 inactivation leads to extra cell divisions without affecting mitosis or cell fate.
- CDC-14 promotes nuclear accumulation of the CKI-1 inhibitor.
Conclusions:
- CDC-14 acts upstream of CKI-1 to promote developmentally programmed cell-cycle arrest.
- CDC-14 stabilizes CKI-1, leading to a hypophosphorylated state required for cell quiescence.
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