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Spatial control of mitosis by the GTPase Ran - Cellular and Molecular Life Sciences

  • ️Lavia, P.
  • ️Sat May 05 2007

Abstract.

Mitosis is the most potentially dangerous event in the life of a cell, during which the cell genetic identity is transmitted to daughters; errors at this stage may yield aneuploid cells that can initiate a genetically unstable clone. The small GTPase Ran is the central element of a conserved signaling network that has a prominent role in mitotic regulation. Pioneering studies with amphibian oocytes indicated that Ran, in the GTP-bound form, activates factors that regulate spindle assembly and dynamics. An increasing body of data indicate higher specificity and complexity in mitotic control operated by Ran in somatic cells. Newly identified target factors of Ran operate with different specificity, and it is emerging that mitotic progression requires the precise positioning of Ran network components and effectors at specific sites of the mitotic apparatus according to a highly regulated schedule in space and time. In this review we summarize our current understanding of Ran control of mitosis and highlight the specificity of mechanisms operating in mammalian somatic cells.

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Authors and Affiliations

  1. CNR National Research Council, Institute of Molecular Biology and Pathology, c/o University ‘La Sapienza’, Via degli Apuli 4, 00185, Rome, Italy

    M. Ciciarello, R. Mangiacasale & P. Lavia

Authors

  1. M. Ciciarello

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  2. R. Mangiacasale

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  3. P. Lavia

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Corresponding author

Correspondence to P. Lavia.

Additional information

M. Ciciarello, R. Mangiacasale: These authors contributed equally to this work.

Received 29 December 2006; received after revision 13 March 2007; accepted 29 March 2007

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Cite this article

Ciciarello, M., Mangiacasale, R. & Lavia, P. Spatial control of mitosis by the GTPase Ran. Cell. Mol. Life Sci. 64, 1891–1914 (2007). https://doi.org/10.1007/s00018-007-6568-2

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  • Published: 05 May 2007

  • Issue Date: August 2007

  • DOI: https://doi.org/10.1007/s00018-007-6568-2

Keywords.