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J Cell Biol. 2010 May 17; 189(4): 614.
PMCID: PMC2872916
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Cdc14 in good repair

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Three hours after irradiation, cells lacking Cdc14A (middle) or Cdc14B (right) retain more DNA damage sites (green) than control cells (left).

Cdc14 is an essential regulator of the yeast cell cycle, but its vertebrate homologues appear to be surprisingly dispensable, Mocciaro et al. report. They are required for efficient DNA repair, however.

Yeast Cdc14 is a phosphatase that counteracts the cyclin-dependent kinases to control many aspects of the cell cycle including mitotic exit. Vertebrates have at least two versions of the phosphatase that have a similarly wide range of functions according to overexpression and depletion experiments. Cdc14A is thought to control centrosome splitting and cytokinesis, for example, while Cdc14B promotes mitotic exit and activates a DNA damage checkpoint that maintains cells in G2.

Mocciaro et al. were thus surprised to find that deleting either phosphatase from chicken DT40 cells had no obvious effect on cell viability or proliferation. And irradiated cells lacking Cdc14A or Cdc14B still arrested in G2. But the knockout cells took longer to repair the radiation-induced DNA damage. Even without irradiation, cells lacking Cdc14A or Cdc14B had higher background levels of double-strand breaks, indicating that the phosphatases are needed to efficiently mend DNA damage. This function isn't unique to chicken cells because genetically deleting either Cdc14 homologue from human cells also slowed DNA repair.

Human cells lacking Cdc14A or Cdc14B were also viable and passed through the cell cycle without any problems. Although the two isoforms localize to different parts of the cell, it's possible that they redundantly carry out the functions of Cdc14 indicated by previous experiments. The authors now plan to test this by generating double knockout cell lines.

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