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FBXW5 controls centrosome number

Nature Cell Biology volume 13, pages 888–890 (2011)Cite this article

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Regulatory mechanisms to prevent centriole overduplication during the cell cycle are not completely understood. In this issue, FBXW5 is shown to control the degradation of the centriole assembly factor HsSAS-6. Moreover, the study proposes that FBXW5 is a substrate of both PLK4 and APC/C, two established regulators of centriole duplication.

Centrioles are fundamental for the assembly of microtubule-based structures, including cilia, flagella and the centrosome1. Abnormalities in centriole structure and function are associated with a number of diseases, including ciliopathies, obesity, primary microcephaly, male sterility and cancer. Not surprisingly, centriole duplication is exquisitely regulated and coordinated with the cell cycle. Each S phase, only one new centriole (termed a procentriole) is assembled from the lateral surface of the two pre-existing centrioles. The procentriole elongates until early mitosis and remains attached to its parental centriole until they disengage (that is, they lose their orthogonal configuration) in late mitosis. It is only after disengagement that centrioles are able to nucleate procentrioles2. In addition, to ensure centriole 'copy number control'1, cells tightly regulate the levels and activity of centriole assembly factors.

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Figure 1: Positive regulators of centriole duplication are regulated by degradation.

References

  1. Nigg, E. A. Trends Cell Biol. 17, 215–221 (2007).

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  2. Tsou, M. F. & Stearns, T. Nature 442, 947–951 (2006).

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  3. Habedanck, R., Stierhof, Y. D., Wilkinson, C. J. & Nigg, E. A. Nat. Cell Biol. 7, 1140–1146 (2005).

    CAS  Article  PubMed  Google Scholar 

  4. Kleylein-Sohn, J. et al. Dev. Cell 13, 190–202 (2007).

    CAS  Article  PubMed  Google Scholar 

  5. Leidel, S., Delattre, M., Cerutti, L., Baumer, K. & Gonczy, P. Nat. Cell Biol. 7, 115–125 (2005).

    CAS  Article  PubMed  Google Scholar 

  6. Kitagawa, D. et al. Cell 144, 364–375 (2011).

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  7. van Breugel, M. et al. Science 331, 1196–1199 (2011).

    CAS  Article  PubMed  Google Scholar 

  8. Strnad, P. et al. Dev. Cell 13, 203–213 (2007).

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  9. Freed, E. et al. Genes Dev. 13, 2242–2257 (1999).

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  10. Piva, R. et al. Mol. Cell Biol. 22, 8375–8387 (2002).

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  11. D'Angiolella, V. et al. Nature 466, 138–142 (2010).

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  12. Guderian, G., Westendorf, J., Uldschmid, A. & Nigg, E. A. J. Cell Sci. 123, 2163–2169 (2010).

    CAS  Article  PubMed  Google Scholar 

  13. Guardavaccaro, D. et al. Dev. Cell 4, 799–812 (2003).

    CAS  Article  PubMed  Google Scholar 

  14. Puklowski, A. et al. Nat. Cell Biol. 13, 1004–1009 (2011).

    CAS  Article  PubMed  Google Scholar 

  15. Kitagawa, D., Busso, C., Fluckiger, I. & Gonczy, P. Dev. Cell 17, 900–907 (2009).

    CAS  Article  PubMed  Google Scholar 

  16. Hatch, E. M., Kulukian, A., Holland, A. J., Cleveland, D. W. & Stearns, T. J. Cell Biol. 191, 721–729 (2010).

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  17. Hu, J. et al. Genes Dev. 22, 866–871 (2008).

    CAS  Article  PubMed  PubMed Central  Google Scholar 

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Affiliations

  1. Julia Pagan and Michele Pagano are in the Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 522 First Avenue, SRB 1107, New York, New York 10016, USA

    Julia Pagan & Michele Pagano

  2. Michele Pagano is at the Howard Hughes Medical Institute, 4000 Jones Bridge Road Chevy Chase, Maryland 20815-6789, USA

    Michele Pagano

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  1. Julia Pagan
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  2. Michele Pagano
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Correspondence to Michele Pagano.

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The authors declare no competing financial interests.

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Pagan, J., Pagano, M. FBXW5 controls centrosome number. Nat Cell Biol 13, 888–890 (2011). https://doi.org/10.1038/ncb2312

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