Recino, A., Sherwood, V., Flaxman, A., Cooper, W. N., Latif, F., Ward, A. and Chalmers, A. D., 2010. Human RASSF7 regulates the microtubule cytoskeleton and is required for spindle formation, Aurora B activation and chromosomal congression during mitosis. Biochemical Journal, 430 (2), pp. 207-213.
RASSF7, a member of the N-terminal Ras association domain family, has increased expression in various cancers and, on the basis of our previous work in Xenopus embryos, may be a regulator of mitosis. In the present study, we address, for the first time, the role of human RASSF7 in mitosis. We demonstrate that RASSF7 is expressed in a broad range of different cell types and that this expression could be enhanced following exposure to hypoxia. Knocking down RASSF7 in human cell lines inhibited cell growth and induced defects in mitosis, including aberrant spindle formation and a failure in chromosomal congression. In order to understand the molecular basis of the defects in more detail, we analysed the activity of mitotic signalling proteins and found that activation of Aurora B did not occur in cells in which RASSF7 was knocked down. We also show that endogenous RASSF7 protein localizes to the centrosome and demonstrate using microtubule-regrowth assays that RASSF7 is an important regulator of microtubule dynamics. On the basis of these observations, we propose that, owing to its key role in regulating the microtubule cytoskeleton, RASSF7 is required for mitosis in human cells.
|Item Type ||Articles|
|Creators||Recino, A., Sherwood, V., Flaxman, A., Cooper, W. N., Latif, F., Ward, A. and Chalmers, A. D.|
|Departments||Faculty of Science > Biology & Biochemistry|
|Research Centres||Centre for Regenerative Medicine|
|Publisher Statement||Recino_et_al_2010.pdf: © 2010 The Author(s) The author(s) has paid for this article to be freely available under the terms of the Creative Commons Attribution Non-Commercial Licence (http://creativecommons.org/licenses/by-nc/2.5/) which permits unrestricted non-commercial use, distribution and reproduction in any medium, provided the original work is properly cited.|
|Additional Information||A.R. was supported by a Marie Curie Ph.D. studentship [grant number MCEST-CT-2005-019822]. F.L. was supported by the Breast Cancer Campaign. A.D.C. was supported by a Medical Research Council Career Development Fellowship [grant number G120/844].|
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