| First Author | Hudson JW | Year | 2001 |
| Journal | Curr Biol | Volume | 11 |
| Issue | 6 | Pages | 441-6 |
| PubMed ID | 11301255 | Mgi Jnum | J:68142 |
| Mgi Id | MGI:1932182 | Doi | 10.1016/s0960-9822(01)00117-8 |
| Citation | Hudson JW, et al. (2001) Late mitotic failure in mice lacking Sak, a polo-like kinase. Curr Biol 11(6):441-6 |
| abstractText | Polo-like kinases in yeast, flies, and mammals regulate key events in mitosis. Such events include spindle formation at G2/M, the anaphase-promoting complex (APC) at the exit from mitosis, the cleavage structure at cytokinesis, and DNA damage checkpoints in G2/M. Polo-like kinases are distinguished by two C-terminal polo box (pb) motifs, which localize the enzymes to mitotic structures. We previously identified Sak, a novel polo-like kinase found in Drosophila and mammals. Here, we demonstrate that the Sak kinase has a functional pb domain that localizes the enzyme to the nucleolus during G2, to the centrosomes in G2/M, and to the cleavage furrow during cytokinesis. To study the role of Sak in embryo development, we generated a Sak null allele, the first polo-like kinase to be mutated in mice. Sak(-/-) embryos arrested after gastrulation at E7.5, with a marked increase in mitotic and apoptotic cells. Sak(-/-) embryos displayed cells in late anaphase or telophase that continued to express cyclin B1 and phosphorylated histone H3. Our results suggest that Sak is required for the APC-dependent destruction of cyclin B1 and for exit from mitosis in the postgastrulation embryo. |
