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First published online 19 May 2009
doi: 10.1242/jcs.036715

Journal of Cell Science 122, 2014-2023 (2009)
Published by The Company of Biologists 2009
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Research Article

{gamma}-Tubulin-containing abnormal centrioles are induced by insufficient Plk4 in human HCT116 colorectal cancer cells

Ryoko Kuriyama1,*, Monica Bettencourt-Dias2, Ingrid Hoffmann3, Marc Arnold3 and Lisa Sandvig1

1 Department of Genetics, Cell Biology and Development, University of Minnesota, Minneapolis, MN 55455, USA
2 Cell Cycle Regulation Laboratory, Instituto Gulbenkian de Ciência, Oeiras, Portugal
3 Cell Cycle Control and Carcinogenesis, German Cancer Research Center, Heidelberg, Germany

* Author for correspondence (e-mail: kuriy001{at}umn.edu)

Accepted 27 February 2009

Cancer cells frequently induce aberrant centrosomes, which have been implicated in cancer initiation and progression. Human colorectal cancer cells, HCT116, contain aberrant centrioles composed of disorganized cylindrical microtubules and displaced appendages. These cells also express unique centrosome-related structures associated with a subset of centrosomal components, including {gamma}-tubulin, centrin and PCM1. During hydroxyurea treatment, these abnormal structures become more abundant and undergo a change in shape from small dots to elongated fibers. Although {gamma}-tubulin seems to exist as a ring complex, the abnormal structures do not support microtubule nucleation. Several lines of evidence suggest that the fibers correspond to a disorganized form of centriolar microtubules. Plk4, a mammalian homolog of ZYG-1 essential for initiation of centriole biogenesis, is not associated with the {gamma}-tubulin-specific abnormal centrosomes. The amount of Plk4 at each centrosome was less in cells with abnormal centrosomes than cells without {gamma}-tubulin-specific abnormal centrosomes. In addition, the formation of abnormal structures was abolished by expression of exogenous Plk4, but not SAS6 and Cep135/Bld10p, which are downstream regulators required for the organization of nine-triplet microtubules. These results suggest that HCT116 cells fail to organize the ninefold symmetry of centrioles due to insufficient Plk4.

Key words: Centrosomes, Centrioles, Nine-triplet microtubules, Hydroxyurea, {gamma}-tubulin, Plk4, SAS6, Cep135, HCT116 cells


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