Ectopic Expression of Plk1 Leads to Activation of the Spindle Checkpoint

• Published in: Cell cycle (Georgetown, Tex.) Vol. 5; no. 21; pp. 2484 - 2488
• Main Authors: Tang, Jiabin, Erikson, Raymond L, Liu, Xiaoqi
• Format: Journal Article
• Language: English
• Published: United States 01.11.2006
• Subjects: Binding; Biology; Bioscience; Calcium; Cancer; Cell; Cell Cycle; Cell Cycle Proteins - biosynthesis; Cell Cycle Proteins - physiology; Cell Proliferation; Cell Survival; Checkpoint Kinase 1; Chromosomes - ultrastructure; Cycle; DNA Damage; Gene Expression Regulation; HeLa Cells; Humans; Landes; Microscopy, Fluorescence; Mitosis; Organogenesis; Phenotype; Polo-Like Kinase 1; Protein Kinases - biosynthesis; Protein Kinases - physiology; Protein Serine-Threonine Kinases - biosynthesis; Protein Serine-Threonine Kinases - physiology; Proteins; Proto-Oncogene Proteins - biosynthesis; Proto-Oncogene Proteins - physiology; RNA Interference; Spindle Apparatus
• ISSN: 1538-4101; 1551-4005
• DOI: 10.4161/cc.5.21.3411

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 co-expression of Chk1 could release this mitotic block. Moreover, the Plk1 expression-induced mitotic block was also released by inactivation of the spindle-assembly checkpoint.