Access

You are not currently logged in.

Access your personal account or get JSTOR access through your library or other institution:

login

Log in to your personal account or through your institution.

If You Use a Screen Reader

This content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.

Human Mps1 Protein Kinase Is Required for Centrosome Duplication and Normal Mitotic Progression

Harold A. Fisk, Christopher P. Mattison and Mark Winey
Proceedings of the National Academy of Sciences of the United States of America
Vol. 100, No. 25 (Dec. 9, 2003), pp. 14875-14880
Stable URL: http://www.jstor.org/stable/3148528
Page Count: 6
  • Read Online (Free)
  • Subscribe ($19.50)
  • Cite this Item
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Human Mps1 Protein Kinase Is Required for Centrosome Duplication and Normal Mitotic Progression
Preview not available

Abstract

The mitotic spindle is essential for the maintenance of genetic stability, and in budding yeast its assembly and function depend on the Mps1 protein kinase. Mps1p is required for centrosome duplication and the spindle checkpoint. Several recent reports demonstrate that vertebrate Mps1 proteins regulate the spindle checkpoint, but reports conflict regarding their role in centrosome duplication. Here we provide multiple lines of evidence that the human Mps1 protein (hMps1) is required for centrosome duplication. A recently described rabbit polyclonal antibody against hMps1 specifically recognizes centrosomes in a variety of human cell types. Overexpression of a dominant-negative version of hMps1 (hMps1KD) can prevent centrosome duplication in a variety of cell types, and active hMps1 accelerates centrosome reduplication in U2OS cells. Finally, we demonstrate that disruption of hMps1 function with pools of hMps1-specific small interfering RNAs causes a pleiotropic phenotype resulting from the combination of severe mitotic abnormalities and failures in centrosome duplication. This approach demonstrates that hMps1 is required for centrosome duplication and for the normal progression of mitosis, and suggests that the threshold level of hMps1 function required for centrosome duplication is lower than that required for hMps1 mitotic functions.

Page Thumbnails

  • Thumbnail: Page 
[14875]
    [14875]
  • Thumbnail: Page 
14876
    14876
  • Thumbnail: Page 
14877
    14877
  • Thumbnail: Page 
14878
    14878
  • Thumbnail: Page 
14879
    14879
  • Thumbnail: Page 
14880
    14880