Polo-like kinase 1 (Plk1), the best characterized member of the mammalian polo-like kinase family, is well regulated throughout the cell cycle, and is inhibited following DNA damage. Chk1 plays a key role in the response to DNA damage. We recently reported that Chk1 is required for mitotic progression through negative regulation of Plk1. Here, we report the phenotypes of cultured cells upon ectopic expression of various forms of Plk1. Epitopic expression of Plk1 led to mitotic arrest, whereas coexpression of Chk1 could release this mitotic block. Moreover, the Plk1 expression-induced mitotic block was also released by inactivation of the spindle-assembly checkpoint.
|Number of pages||5|
|State||Published - Nov 1 2006|
Bibliographical noteFunding Information:
We thank Eleanor Erikson for critical reading of this manuscript, and David Stern for the HA-Chk1 construct. This work was supported by National Institutes of Health Grant GM59172. R.L.E. is the John F. Drum American Cancer Society Research Professor. X.L. is a recipient of the Howard Temin Award from the National Cancer Institute (K01 CA114401).
- Cell cycle
- Chromosome congression
- Spindle checkpoint
ASJC Scopus subject areas
- Molecular Biology
- Developmental Biology
- Cell Biology